Neurology Update (Khalil) PDF
Document Details
Uploaded by DelightedEnlightenment8534
Khalil
Tags
Summary
This document provides a summary of different neurological conditions and their related aspects, discussing various topics like CSF production, intracranial pressure, different types of hernias, examination procedures, and specific diseases (brain metastases, gliomas, meningiomas, etc.).
Full Transcript
1. It can be said about the production of CSF: A) Production is dependent on carbonic anhydrase B) The total volume of CSF in the skull and spinal canal is approx. 150 ml C) It is independent of the Na+/K+ pump D) It is produced in arachnoid villi E) The total volume in the skull and spinal canal is...
1. It can be said about the production of CSF: A) Production is dependent on carbonic anhydrase B) The total volume of CSF in the skull and spinal canal is approx. 150 ml C) It is independent of the Na+/K+ pump D) It is produced in arachnoid villi E) The total volume in the skull and spinal canal is about 450 ml F) The total CSF volume is completely replaced 5 times a day G) Produce approximately 10 ml/min. H) The total CSF volume is completely replaced 3 times a day I) Produce approximately 0,3 ml/minute J) It is mainly produced in the choroid plexus 2. The Monroe-Kellie Law refers to: A) Intracranial pressure self-regulation B) Linear increase of PIC to any change in intracranial volume C) The exponential increase in PIC after the clearing threshold has been reached D) The relationship between intracranial pressure and heart rate E) The relationship between intracranial pressure and consciousness F) In an inextensible space the appearance of an additional volume allows the PIC to be maintained until the compensatory mechanisms are exceeded G) The relationship between intracranial pressure and oxygen saturation H) The inability of the brain to compensate for any change in intracranial volume in an inextensible space I) The buffer capacity of the CSF as a compensation mechanism J) The relationship between intracranial pressure and brain compensation capabilities 3. Cerebral perfusion pressure: A) The normal range is typically 25-45 mm Hg B) It is due to the difference between systolic blood pressure and intracranial pressure C) This is due to the difference between average blood pressure and intracranial pressure D) It is due to the difference between diastolic blood pressure and intracranial pressure E) This is an important prognostic factor F) When it falls below 45 mm Hg, the risk of ischemia occurs G) It is given by the difference between mean blood pressure and intracranial pressure divided by 2 H) The normal range is typically 55-65 mm Hg I) Normal < 50 mm Hg J) Normal > 50 mm Hg 4. Brain hernias can be of the following types: A) sphenoidal B) bone defect (craniotomy or traumatic defect) C) subfalciform D) ethmoidal E) extradural F) tonsilar G) ascending central H) intraventricular I) transstentorial J) subdural 5. Neurological examination of the patient with HIC syndrome should include: A) Cranial nerves B) Motor and reflex function C) Cardiac status D) Respiratory function E) Sensory function F) Determination of Glasgow score in the traumatic patient G) Digestive function H) Psychological status I) The sphincter function J) Mental status 6. Glasgow coma scale: A) Appreciate the verbal, motor, sensitive response B) The score can be between 0 and 15 C) The score can be between 3 and 15 D) Appreciate the eye, motor, verbal response E) It may be a prognostic indicator F) This is not an indicator of prognosis G) It doesn't correlate with the degree of the coma H) It correlates with the degree of coma I) A patient can be considered comatose at a score < 7 J) A patient is considered comatose at a score ≤ 8 7. Regarding brain metastases, it can be said that: A) It accounts for about half of the number of primary tumors B) Symptoms due to brain metastases lead to the initial discovery of primary cancer in 30% of cases C) Melanoma is the most common neoplasia that gives multiple brain metastases D) Symptoms due to brain metastases lead to the initial discovery of primary cancer in 15% of cases E) Lung cancer is the most common neoplasia that produces multiple brain metastases F) The most common are those with starting point lung cancer G) They are more common than primary brain tumors H) Melanoma, coriocarcinoma, renal cell carcinoma and thyroid carcinoma are the most common neoplasms that present with an intratumoral hemorrhage I) The most common are those with starting point breast carcinoma J) Metastases of pulmonary origin are most commonly presented by intra-tumoral hemorrhage 8. Regarding primary brain tumors, the following can be stated: A) They are more common than brain metastases B) All primary lymphomas of the CNS are malignant C) All primary CNS lymphomas are benign D) Primary intracranial intraparenchymal tumors are more common than extraparenchymal tumors E) They are less common than brain metastases F) Primary extraparenchymal intracranial tumors are more common than intraparenchymal tumors G) Most extraparenchymal tumors are benign H) Most extraparenchymal tumors are malignant I) Primary parenchymal tumors are predominantly malignant J) Primary intraparenchymal tumors are predominantly benign 9. As for brain gliomas, the following statements are true: A) The average survival in glioblastoma multiforme is 5 years B) The median survival in glioblastoma multiforme is 12-13 months C) Malignant gliomas rarely metastasize D) Glioblastoma multiforme is one of the most aggressive malignant tumors of the brain E) Juvenile pilocytic astrocytoma is one of the most aggressive brain tumors F) Include astrocytoma, oligodendroglioma, oligoastrocytoma, ependymoma G) Astrocytomas are also called glioblastomas H) Include meningioma, schwanoma, pituitary adenoma, craniopharyngioma I) Malignant gliomas metastasize frequently J) Grade IV astrocytoma is known as glioblastoma multiforme. 10. Intracranial meningiomas: A) The degree of resection is defined on the Simpson scale B) They are vascularized by meningeal branches in ACE C) It doesn't interest the adjacent bone D) They are born in arachnoid “cap-cells” E) They do not benefit of radiation therapy F) They are predominantly malignant tumors G) They're vascularized by branches in the anterior cerebral artery H) They are born from the cells of the dura mater I) They are predominantly benign tumors J) May involve adjacent bone (hyperostosis) 11. Vestibular Schwanomas: A) Representsthe second in frequency between schwanomas of cranial nerves after trigeminal schwanoma B) May affect the cranial nerves III, IV, VI, VII, VIII. C) They are born from the Schwann cells of the acoustic component of nerve VIII, which is why they are also called acoustic neuromas D) May affect by their growth the cranial nerves VIII, VII, V, XI, X E) Microsurgery is the only treatment option F) These are the most common cranial nerve schwanomas G) They are often bilateral H) Stereotactic radiosurgery is an alternative to microsurgical resection for tumors up to 3-3,5 cm in diameter I) Unilateral tumors occur sporadically, and bilateral tumors occur in neurofibromatosis type 2 J) They are born from the Schwann cells of the vestibular component of the VIII nerve 12. The following statements are true in the case of pituitary adenomas: A) The most common form of functional pituitary adenoma is prolactinoma B) Apparently complete surgical resection of macroadenomas is possible in about 85% of cases C) The only treatment option is transsphenoid or transcranial surgical resection D) They are classified as microadenomas ( 3 cm diameter) H) The most common form of functional pituitary adenoma is somatotrop adenoma, which causes acromegaly I) All adenomas secrete hormones – somatotrop, ACTH, gonadotropes J) They may be functional (hormone-secreting) or non-functional 13. The germs most involved in bacterial infectious meningitis are: A) Streptococcus pneumoniae (pneumococul), Haemophilus ifluenzae, Neisseria meningitidis, Staphylococcus aureus B) Meningitis with Streptococcus pneumoniae is more common in young children C) Meningitis with H. influenzae is most common in young children D) Gram negative Bacilli should be considered in infants (< 1 month) E) Meningitis with Neisseria meningitidis and Streptococcus pneumoniae is more common in adolescents and young adults F) Gram positive Bacilli should be considered in infants ( 6 weeks) 165. The following statement about the positive diagnosis in the case of myelitis are true: A) Spinal cord MRI shows T2 sequence hypodensity at the level of the lesion B) Sensory problemsoccur in the form of a syringomyelia sensory dissociation syndrome C) Bowel and bladder dysfunctions are characterized by involuntary leakage of urine and faeces D) In the medullary shock phase, deep tendon reflexes and cutaneous reflexes are abolished, but the Babinski sign is present E) Moderate fever occurs as an initial symptom F) Trophic problems are represented by edema, blisters and skin ulcers G) The onset is characterized by rachialgia, with pain „in the belt” H) No trophic or vasomotor disturbances occur I) CSF examination does not provide relevant information for diagnosis J) Motor and sensory deficits occur from a few hours to 1-3 days after pain, dysuria and fever 166. The following statement about the diagnosis and evolution of myelitis are true: A) CSF analysis in myelitis sanguine or xanthochromic macroscopic aspect B) Myelography and electrophysiological studies are of limited utility C) Contrast-enhanced MRI is of limited utility for the diagnosis of myelitis D) In case of incomplete section, after the state of medullary shock, the phenomena of medullary automatism appear E) Very frequently, the evolution of myelitis acquires an ascending character, including the the midbrain F) Routine blood tests are within normal limits and of no benefits for diagnostic G) CSF examination in myelitis reveals mild or moderate pleocytosis H) In the phase of medullary automatism post acute myelitis, deep tendon reflexes are exaggerated, with the presence of defensive reflexes and bilateral Babinski sign I) After a transverse myelitis, although the section has been total and definitive, motor and sensory deficits will gradually improve J) In the case of a complete and definitive spinal cord section, motor and sensory deficits are irreversible 167. The following statements about the therapeutic approach to the patient with myelitis are true: A) In the acute phase, the treatment is symptomatic along with hygienic and dietary measures to prevent complications B) The presence of superinfected skin ulcers, bowel and bladder dysfunctions suggests a poor long-term prognosis C) After establishing the etiology, the treatment of the underlying disease begins with corticotherapy, antibiotic therapy, immunotherapy D) The treatment of choice in the acute phase is surgery E) Passive physical therapy can be initiated at bedsidestarting from the acute phase if the patient's condition allows F) Passive physical therapy should not be started in the acute phase G) Currently, guidelines recommend the implantation of spinal cord stimulation devices to supplement impaired functions H) Patients who remain only with sensory disturbances have a worse long-term prognosis I) Long term treatment consist of periodic and sustained physical therapy J) Pulmonary drainage measures are not recommended in patients with myelitis 168. Regarding amyotrophic lateral sclerosis (ALS) the following statements are TRUE: A) It is a degenerative disease B) The average life expectancy after diagnosis is 3 years C) There are only familial forms of ALS D) The average life expectancy after diagnosis is 20 years E) Both central and peripheral motor neurons are affected F) It is an autoimmune disease G) It can be sporadic or familial H) The symptomatology is progressive I) It is characterized by relapses and remissions J) Both sensory and motor neurons are affected 169. The following statements regarding the clinical picture in amyotrophic lateral sclerosis (ALS) are TRUE: A) The lower limbs are never involved in ALS and the patient has no difficulty walking B) It reveals the association between progressive motor deficit and amyotrophies C) It reveals the association between progressive motor deficit and muscular hypertrophy D) The presence of amyotrophies and fasciculations proves the involvement of the lower motor neuron E) The motor deficit can be accompanied by hyperreflexia, spasticity and pathological reflexes F) The presence of amyotrophies and fasciculations proves the involvement of the upper motor neuron G) The bulbar involvement is only noticed later in the evolution of the disease. It cannot be present at onset. H) Hyperreflexia, spasticity and pathological reflexes cannot be part of the clinical picture in ALS I) It can present with bulbar onset J) The involvement of the lower limbs is signaled by falls, decreased walking distance and walking instability 170. The following statements regarding the clinical picture in amyotrophic lateral sclerosis (ALS) are TRUE: A) Fasciculations may not be present from the beginning B) The bulbar involvement is signaled by problems with deglutition and phonation C) Spasticity is usually present D) Spasticity is usually absent E) Deglutition problems increase the risk of aspiration pneumopathy F) Deglutition problems do not increase the risk of aspiration pneumopathy G) The bulbar involvement is signaled by hearing loss and the presence of vertigo H) The abnormal usage of joints does not cause pain or induce deformities I) The complete absence of fasciculations throughout the course of the disease is not a red flag for reconsidering the diagnosis J) The abnormal usage of joints can cause pain or induce deformities 171. Regarding amyotrophic lateral sclerosis (ALS) the following statements are TRUE: A) The cellular loss is located in the sensory cortex, the posterior horns of the spinal cord and the sensory nuclei of the cranial nerves B) The administration of riluzole cures ALS C) The average life expectancy after diagnosis is 3 years D) The incidence is higher between the ages of 65 and 74 years old E) The incidence is higher between the ages of 25 and 34 years old F) The cellular loss is located in the motor cortex, the anterior horns of the spinal cord and the motor nuclei of the cranial nerves G) There is no cure or effective treatment for ALS H) It is also known as Lyme disease I) It is also known as Lou Gehrig’s disease J) The average life expectancy after diagnosis is 20 years 172. Regarding amyotrophic lateral sclerosis (ALS) the following statements are FALSE: A) Both central and peripheral motor neurons are affected B) There are only familial forms of ALS C) The symptomatology is progressive D) It is an autoimmune disease E) It is a degenerative disease F) Both sensory and motor neurons are affected G) The average life expectancy after diagnosis is 3 years H) It is characterized by relapses and remissions I) It can be sporadic or familial J) The average life expectancy after diagnosis is 20 years 173. Regarding the paraclinical investigations used for diagnosing amyotrophic lateral sclerosis (ALS) the following statements are TRUE: A) Muscle biopsy is useful for distinguishing between a neurogenic disorder (such as ALS) and a primary muscle disease (myopathy) B) Blood tests are not usually performed in ALS C) The EMG (electromyography) exam reveals fasciculation potentials, which are characteristic for this disease D) Nerve conduction velocities are increased E) Blood tests which include CBC and CK are usually performed F) The EMG exam reveals fasciculation potentials, which are not characteristic for this disease G) Nerve conduction velocities can be either normal or slightly diminished H) Muscle biopsy is not useful for distinguishing between a neurogenic disorder (such as ALS) and a primary muscle disease (myopathy) I) MRI findings are ALS specific and they usually show frontoparietal cortical atrophy J) MRI findings are not ALS specific and they usually show frontoparietal cortical atrophy 174. The following statements regarding the therapeutical approach in amyotrophic lateral sclerosis (ALS) are TRUE: A) A multidisciplinary team should be involved B) The symptomatic treatment of ALS is meant to improve the patient’s quality of life C) The symptomatic treatment of ALS addresses problems such as sialorrhea, pain, bronchi secretions, cramps, spasticity, depression, anxiety and insomnia D) An unidisciplinary team should be involved E) There are no therapeutical options to address spasticity in ALS F) The symptomatic treatment of ALS is meant to improve the patient’s sensory deficit G) There are no therapeutical options to address sialorrhea in ALS H) The administration of riluzole cures ALS I) Riluzole increases life expectancy by 3 months after 18 months of treatment J) The only treatment with a neuroprotective effect is riluzole 175. The symptomatic treatment in amyotrophic lateral sclerosis (ALS) usually addresses the following problems: A) Pain B) Sialorrhea C) Hyperhidrosis D) Hearing loss E) Visual disturbance F) Depression, anxiety and insomnia G) Bradykinesia H) Sensory deficit I) Spasticity and cramps J) Bronchi secretions 176. The following statements regarding syringomyelia are TRUE: A) Pyramidal signs can be identified below the level of the lesion B) It is defined by the presence of one or more cavities mainly in the cervical region C) It affects the spinal cord D) Characteristic to this disease is the loss of pain and temperature sensations and the presence of muscle atrophies in the upper limbs E) It affects the basal ganglia F) Pyramidal signs can be identified at the level of the lesion G) Characteristic to this disease is the loss of proprioception and vibratory sensation and the presence of muscle atrophies in the upper limbs H) Syringomyelia is a degenerative disorder I) It is defined by abnormal protein folding and aggregation mainly in the basal ganglia J) Syringomyelia is an autoimmune disorder 177. Syringomyelia can be caused by: A) Hematomyelia B) Radiation myelopathy C) Spinal cord ischemia D) Lyme disease E) Trauma F) Herniated disks G) Autoimmune myelopathies H) Copper deficiency myelopathy I) Extramedullary tumors J) Intramedullary tumors 178. The following statements regarding the clinical picture in syringomyelia are TRUE: A) The patient presents with loss of proprioception and vibratory sensation and amyotrophies in the upper limbs B) Symptoms usually begin between 65 and 75 years old C) As the diseases progresses, gait disturbances and bulbar dysfunction occur D) The onset is insidious E) The gait disturbances and bulbar dysfunction are usually present at onset F) Both males and females are equally affected G) The patient presents with loss of temperature and pain sensations and amyotrophies in the upper limbs H) Symptoms usually begin between 25 and 35 years old I) Only males are affected J) There is a sudden onset 179. The following statements regarding syringomyelia are TRUE: A) Involvement of the dorsal columns leads to the development of pyramidal signs below the level of the lesion B) The extension of the cavity towards medulla oblongata causes tongue paralysis, dysarthria and problems with deglutition C) The disease usually progresses slowly D) The formation and enlargement of the central spinal cord cavity leads to the interruption of the crossing vibration and proprioception fibers and the patient presents with sensory dissociation E) The majority of cases become severely disabled within 3 to 5 years from symptom onset F) Involvement of the lateral columns leads to the development of pyramidal signs below the level of the lesion G) A few cases become severely disabled within 3 to 5 years from symptom onset H) The disease usually progresses rapidly I) Medulla oblongata is never involved in syringomyelia J) The formation and enlargement of the central spinal cord cavity leads to the interruption of the crossing pain and temperature fibers and the patient presents with sensory dissociation 180. The following statements regarding syringomyelia are TRUE: A) There is no medical or surgical treatment for syringomyelia B) Axial computed tomography and MRI exams cannot detect the cavity C) X-rays of the skull are never part of the diagnostic workup of a patient with syringomyelia D) There are 10 major types of syringomyelia E) There is a unified theory regarding the etiology of this disease F) There are multiple theories regarding the etiology of this disease G) There are 4 major types of syringomyelia H) Axial computed tomography and MRI exams are able to detect the cavity I) Treatment is surgical and aimed at decompressing the foramen magnum and upper cervical spinal canal J) X-rays of the skull are needed to detect platybasia or basilar invagination 181. Regarding the complications of migraine, it can be stated: A) Migraine status is characterized by migraine episodes lasting more than 72 hours B) Migrainous status is characterized by a maximum duration of 72 hours C) Epileptic seizures can occur more than an hour after the migraine attack D) Chronic migraine is characterized by a history of migraine without aura E) Chronic migraine is characterized by a history of migraine with aura F) Migraine attacks can last maximum 15 days G) Migraine doubles the risk of stroke H) Migraine attacks can last more than 15 days and up to 3 months I) Epileptic seizures can be triggered by migraine J) Migraine attacks can last more than 3 months 182. Among the general non-pharmacological measures of migraine treatment, there are: A) Avoiding medication with vasodilatory action B) Avoiding the administration of oral contraceptives C) Methods of autogenous training through biofeed-back D) Avoiding medication with vasoconstrictor action E) There is no warning regarding the administration of contraceptives F) Avoiding alcohol, chocolate, caffeinated products G) During the migraine attack-rest in a bright room H) Consumption of caffeinated products and chocolate I) Avoiding hypoglycemia, fatigue and excessive physical effort J) Avoiding hyperglycemia, fatigue and excessive physical effort 183. Migraine crisis treatment: A) The aim of the treatment is to remove the headache 2-4 hours after administration B) The antimigraine treatment is not adapted according to the intensity of the symptoms C) Triptans are administered as soon as the first signs of a headache attack appear D) The antimigraine medication is administered after the onset of the cephalalgic crisis E) Triptans are effective in early administration F) Triptans have not proven effective in early administration G) Monitoring and eliminating the tendency to self-medicate with overdose H) Antimigraine medication is administered from the first signs of a cephalalgic crisis I) The antimigraine treatment is not adapted according to the accompanying of the vegetative phenomena J) Triptans are administered after the onset of the headache 184. In the form of migraine with mild headache, we can give: A) Nonsteroidal anti-inflammatory medication B) For digestive phenomena, Domperidone 10-40mg/day is associated C) For digestive phenomena, Metoclopramide 10-30mg/day is associated D) Acetylsalicylic acid alone or in medicinal combination E) Acetylsalicylic acid only in drug combination F) Steroidal anti-inflammatory medication G) For digestive phenomena, Metoclopramide isn’t an option H) Naproxen sodium 250mg every 6 hours I) Acetylsalicylic acid is not recomanded J) Do not administrate Naproxen sodium 185. In severe forms of migraine, it is possible to administrate: A) Dihydroergotamine-maximum 2mg/day B) Triptans are contraindicated in severe forms C) Antiemetics are contraindicated in migraine D) Dihydroergotamine - more than 12 hours after the last dose of triptans E) Dihydroergotamine - more than 24 hours after the last dose of triptans F) Ergot derivatives are contraindicated in severe forms G) Ergot derivatives H) Triptans I) Antiemetics (Metoclopramide 10mg) J) Dihydroergotamine is administered immediately after triptans 186. Prophylactic treatment of migraine: A) It is necessary if the severity of the migrenous crisis affects the patient's quality of life B) The majority of prophylactic agents have the same effect compared to placebo C) It is necessary if the patient has only one migraine attack in a month D) It aims to reduce the frequency and intensity of migraine attacks E) It is necessary if the patient has more than 2 migraine attacks in a month F) Obvious results will be obtained after 3-4 months of treatment G) The use of therapeutic agents is recommended for an interval of 3 months H) The results will be obtained after one month of treatment I) It aims to prevent chronicity J) It does not prevent chronic migraine 187. Paraclinical investigations in migraine are: A) There are no paraclinical investigations specific to migraine B) CT and MRI examinations are performed routinely C) CT and MRI are not indicated for the exclusion of an expansive intracranial process D) CT and MRI examinations will be indicated to rule out a subarachnoid hemorrhage E) There are paraclinical investigations specific to migraine F) CT and MRI examinations are not routinely indicated in typical migraine G) Paraclinical investigations are necessary only to exclude an acute organic cause H) CT and MRI examinations will be indicated to rule out an expansive intracranial process I) CT examination is not indicated for the exclusion of a subarachnoid hemorrhage J) Paraclinical investigations are not performed to rule out an acute organic cause 188. The causes incriminated in the determinism of cerebral infarction associated with migraine are: A) Arterial spasm with short duration B) Arterial dissection through repeated and prolonged vasospasm C) Platelet aggregation D) Absence of edema of the vascular walls E) Edema of the vascular walls F) Absence of platelet aggregation G) Absence of prolonged arterial spasm H) Prolonged arterial spasm I) Coagulability changes J) Absence of coagulability changes 189. Migraine triggers can be: A) Stress, emotions, sleep deprivation B) Extreme variations in the external environment (light, noise, smells) C) Prolonged intellectual effort D) Smoking, physiological states E) Prolonged intellectual effort relieves migraine F) Stress and emotions are not migraine triggers G) Sleep deprivation cannot trigger a migraine attack H) Alcohol is not a trigger I) Changes in atmospheric pressure do not influence the triggering of a migraine episode J) Some types of food (alcohol, chocolate) 190. Migraine without aura can be characterized by: A) It has a low recurrence rate B) Moderate to severe headache C) It has an increased rate of recurrence D) Headache of low intensity E) Duration of crisis between 4-72 hours F) The least common form in medical practice G) The most common form in medical practice H) The duration of the crisis between 1-2 hours I) The headache cannot be unilateral J) The headache can present: unilateral location + pulsatility 191. Due to the overload of the central nervous system, in migraine, a series of cascade events occur: A) Increased locus coeruleus nucleus activity with decreased noradrenaline release B) Frequent repetition of migraine attacks does not produce a progressive alteration of the periaqueductal gray matter C) An overload of brainstem mechanisms D) Decreased dorsal raphe nucleus activity with increased serotonin release E) Electrical depression at the level of the occipital lobe underlies the manifestations of migraine aura F) Increased dorsal raphe nucleus activity with decreased serotonin release G) The frequent repetition of migraine attacks produces a progressive alteration of the periaqueductal gray matter - determining the chronicity of the headache H) Increased dorsal raphe nucleus activity with increased serotonin release I) Increased activity of the locus coeruleus nucleus with increased noradrenaline release J) The electrical depression at the level of the frontal lobe is the basis of the manifestations of the migraine aura 192. Migraine with aura can be characterized by: A) It presents a higher frequency than migraine without aura B) It sometimes alternates with episodes of migraine without aura C) The aura is fully reversible within 12 hours D) The aura can be defined by scintillating, extensive, dynamic scotomas E) The aura always appears after the onset of the cephalalgic attack F) Aura can be defined by homolateral visual hemifield disturbances G) The aura usually precedes the cephalalgic attack H) It presents a lower frequency than migraine without aura I) The aura never precedes the cephalalgic attack J) It never alternates with episodes of migraine without aura 193. Prophylactic therapeutic agents for migraine include: A) Beta-blockers (Metorpolol, Atenolol) B) Tricyclic antidepressants (Amitriptyline, Doxepin) C) Tricyclic antidepressants act on the anxiety-depressive component that accompanies the migraine attack D) Anticonvulsant treatment is not part of prophylactic migraine therapy E) Calcium channel blockers are not indicated in patients with migraine infarction F) Calcium channel blockers are contraindicated in migraine prophylaxis G) Anticonvulsant medication (valproic acid, gabapentin, topiramate) H) Calcium channel blockers (Verapamil, Amlodipine) I) Metoprolol is contraindicated in migraine attack prophylaxis J) Amitriptyline does not act on the anxiety-depressive component that accompanies the migraine attack 194. Homonymous hemianopsia: A) Occurs on the same side as the lesion B) Occurs in lesions of the optic pathway at the level of the optic nerve C) Occurs in lesions of the optic pathway at the level of the optic band D) Occurs in lesions of the optic pathway at the level of the lateral geniculate body E) Represents loss of vision in the left or right half of both visual fields F) Occurs in lesions of the optic chiasm G) Represents complete loss of vision in one eye H) Occurs in retinal lesions I) Appears in lesions of the optic path at the level of Gratioletradiation J) Occurs on the opposite side of the lesion 195. The changes that may appear during the fundus examination are: A) Primitive optic atrophy B) Papilledema C) Papillary stasis D) Corneal ulcer E) Uveitis F) Cataract G) Acute inflammation of the anterior portion of the optic nerve H) Acute inflammation of the posterior portion of the optic nerve I) Papillitis J) Chorioretinitis 196. Common oculomotor nerve (III) palsy is characterized by: A) Bilateral drooping of the eyelids in the evening B) Inability to move the eyeball upwards, downwards and inwards C) Palpebral ptosis D) Divergent strabismus E) Lagophthalmia F) Mydriasis G) Inability to move the eyeball outwards H) Bilateral drooping of the eyelids in the evening I) Miosis J) Diplopia 197. The following statements are true: A) The common oculomotor nerve innervates the orbicularis oculi muscle B) The abducens nerve innervates the external rectus muscle C) The common oculomotor nerve innervates the levator eyelid muscle D) The common oculomotor nerve innervates the internal rectus muscle E) The common oculomotor nerve innervates the external rectus muscle F) The abducens nerve innervates the levator eyelid muscle G) The abducens nerve innervates the rectus internus H) The trochlear nerve innervates the external rectus muscle I) The common oculomotor nerve innervates the superior rectus muscle J) The trochlear nerve innervates the superior oblique muscle (large oblique) 198. The trigeminal nerve innervates from a sensory point of view: A) Scalp in the neck region B) Upper lip C) Integuments of the throat D) Upper lip E) Anterior 2/3 of tongue for taste F) Forehead to vertex G) Nasal wing H) Retina I) Posterior 1/3 of tongue for taste J) Cornea 199. From a motor point of view, the trigeminal nerve innervates the following muscles: A) Levator palpebrae B) Scalenus anterior C) Masticatory muscles D) Mylohyoid E) Orbicularis F) Tensor tympani G) Anterior belly of digastric H) Sternocleidomastoideus I) Trapezius J) Temporalis 200. In facial nerve palsy of the peripheral type we meet: A) Dysarthria B) Deletion of front folds C) The patient cannot swallow solid food D) Diplopia E) Erasing the nasolabial fold on the affected side F) Dropping of the mandible G) The patient cannot raise the upper eyelid H) Absence of blinking I) When the patient tries to close the eye on the affected side the eyeball moves upwards and outwards J) When the patient tries to close the eye on the affected side the eyeball moves upwards and outwards 201. In facial nerve palsy of the peripheral type we meet: A) Lagophthalmia B) Deviation of the buccal commissure from the healthy side C) Mydriasis D) Lagophthalmia E) Trismus F) Decreased taste in posterior 1/3 of tongue G) Anosmia H) Epiphora I) Decreased taste in the anterior 2/3 of the tongue J) Amaurosis 202. In facial nerve palsy of the central type we meet: A) The patient cannot raise the eyebrow B) Absence of blinking C) There is a risk of corneal ulcer D) Falling of the buccal commissure with its deviation from the healthy side E) Clinical manifestations only in the lower half of the affected hemiface F) The patient cannot blow or whistle G) Erasing the nasolabial fold H) Deviation of the tip of the tongue to the side of the lesion I) Erasing front pleats J) It can be associated with hemiplegia on the same side 203. Complications of peripheral facial nerve palsy are: A) Epileptic seizures B) Lateral nystagmus C) Facial hemispasm D) Remaining motor deficit in paralyzes with unfavorable evolution E) Calcifications of facial muscles F) Paroxysmal involuntary contractions on small areas at the level of the affected hemiface G) Crocodile tears syndrome with homolateral hyperlacrimation triggered by eating H) Heteronymous hemianopsia I) Corneal ulcerations due to lagophthalmos due to the lack of protection of the eyeball J) Atrophy of the lingual muscles with wrinkled appearance of the lingual mucosa remaining intact 204. Peripheral vestibular syndrome consists of: A) Papillary stasis B) Bilateral mydriasis C) Auditory accusations D) Intense, even paroxysmal vertigo E) Tonic deviations of the head and arms towards the injured side F) Diplopia G) Aguezie H) Horizontal nystagmus I) Ebrios (drunk) gait J) Accentuated vegetative disorders 205. Glossopharyngeal nerve palsy is manifested by: A) Hypo or anesthesia in the posterior pharynx B) The sign of the curtain (when pronouncing the vowel A or E, the movement of the back wall of the pharynx and the palatine veil towards the right side is highlighted C) Dropped shoulder D) Aguezia in anterior 2/3 of tongue E) Hypo or aguesia in the posterior 1/3 of the tongue F) Dysphagia for liquids G) Embarrassment when swallowing solids H) Deviation of the tip of the tongue to the side of the lesion I) Decrease or abolition of the pharyngeal reflex J) Hypophony 206. The vagus nerve ensures, through its preganglionic parasympathetic fibers, the innervation of the following structures: A) Lungs B) Small intestine and part of large intestine. C) Bladder D) Salivary glands E) Pupil F) Prostate G) Myocardium H) Lungs I) Stomach J) Lacrimal gland 207. The cranial nerves originating in the cerebral bulb (medulla oblongata) are: A) Accessory nerve B) Vagus nerve C) Optic nerve D) Trigeminal nerve E) Optic nerve F) Glossopharyngeal nerve G) Hypoglossal nerve H) Spinal nerve (XI) I) Olfactory nerve J) Abducens nerve 208. Bilateral hypoglossal lesions present with: A) Chewing disorders B) Swallowing disorders C) Dyspnea with orthopnea D) Impossibility of tongue protrusion E) Bilateral dropped shoulder F) Complete paralysis of the tongue G) Motor aphasia H) Global atrophy of the tongue with diffuse fasciculations I) Vomiting J) Aguezie for bitter 209. The most common causes of coma are: A) Drugs and toxins B) Multiple sclerosis C) Guillain-Barre syndrome D) Stroke and CNS infections E) Metabolic disorders F) Trauma G) Transverse myelitis H) Neurofibromatosis type 1 I) Amyotrophic lateral sclerosis J) Mass lesions 210. The assessment of brainstem function in the unconscious patient includes: A) Testing the plantar reflex B) Performing the Rinne and Weber tests C) Testing the corneal reflex D) Assessing eye movements and position E) Testing deep tendon reflexes F) Testing coordination G) Testing the gag/cough reflex (via endotracheal tube if intubated) H) Recording the size and reaction to light of the pupils I) Testing two-point discrimination and stereognosis J) Assessing the respiratory drive 211. The following aspects represent lateralizing signs in the comatose patient: A) Symmetrical response to painful stimuli B) Asymmetry of face C) Symmetry of decerebrate and decorticate posturing D) Symmetry of tone E) Asymmetry of tone F) Asymmetrical response to painful stimuli G) Symmetry of face H) Asymmetry of tendon reflexes and plantar responses I) Symmetry of tendon reflexes and plantar responses J) Asymmetry of decerebrate and decorticate posturing 212. The following investigations are part of the diagnostic workup of a comatose patient: A) CSF examination – routinely; it is not contraindicated even if an intracranial mass lesion is a possibility B) Metabolic and endocrine studies C) CSF examination – only after careful risk assessment; it is contraindicated when an intracranial mass lesion is a possibility D) Drug screen and biochemical analysis of the blood E) Arterial blood gases F) Visual evoked potentials G) Brain imaging H) Nerve conduction studies I) Muscle biopsy J) Skin biopsy 213. The following statements regarding vegetative state are TRUE: A) There are signs of awareness and the patient responds to environmental stimuli B) Brainstem function is intact so breathing is normal without the need for mechanical ventilation C) Brainstem function is affected D) There are no signs of awareness or response to environmental stimuli, except reflex movements E) The patient appears awake with eye-opening and sleep-wake cycles F) Is usually a consequence of extensive cortical damage G) It is considered permanent vegetative state if there is no recovery after 12 months when trauma is the cause, and after 6 months for all other causes H) Mechanical ventilation is needed I) Is usually a consequence of focal cortical damage J) It is considered permanent vegetative state if there is no recovery after 24 months when trauma is the cause, and after 16 months for all other causes 214. The following statements regarding Broca’s aphasia are TRUE: A) Broca’s aphasia is characterized by loss of the ability to produce language B) Severe lesions generate abnormalities such as laconic speech, lack of spontaneity, agrammatism, loss of fluency and perseveration of speech C) Broca’s aphasia is characterized by loss of the ability to understand language D) In a recovering patient, the first to reappear are the short, habitual phrases (“hi”, “yes”, “no”, counting or naming the days of the week) E) Less severe lesions generate abnormalities such as laconic speech, lack of spontaneity, agrammatism, loss of fluency and perseveration of speech F) The lesions leading to Broca’s aphasia may also involve parts of the insular and motor cortex G) It is caused by lesions of the areas 44 and 45 of the non-dominant hemisphere H) The lesions leading to Broca’s aphasia may also involve parts of the visual and auditory cortex I) It is caused by lesions of the areas 44 and 45 of the dominant hemisphere J) In a recovering patient, the first to reappear are the complex phrases 215. Patients with less severe lesions of Broca’s area present with: A) Lack of spontaneity B) Agrammatism C) Laconic speech D) Elaborate speech E) There is no perseveration of speech F) Spontaneity G) Loss of fluency H) Grammar is not impaired I) The patient retains fluency J) Perseveration of speech 216. The following statements regarding Wernicke’s aphasia are TRUE: A) The patient is unable to understand what is said to him B) The patient is able to read C) It is caused by lesions of the supramarginal and angular gyri (areas 37, 39, 40) and the posterior part of the superior temporal gyrus (area 22) of the dominant hemisphere D) The patient is unable to read (alexia) E) The patient has a fluent and paraphasic speech F) The patient is able to write G) The patient is unable to produce written language (agraphia) H) The patient has a non-fluent speech I) It is caused by lesions of the areas 44 and 45 of the dominant hemisphere J) It is characterized by loss of the ability to produce language 217. The following statements regarding Wernicke’s aphasia are TRUE: A) It is characterized by loss of the ability to produce language B) The patient is unable to understand what is said to him C) It is characterized by fluent speech D) It is also called sensory aphasia E) The patient has a non-fluent speech F) It is also called motor aphasia G) It is caused by lesions of the supramarginal and angular gyri (areas 37, 39, 40) and the posterior part of the superior temporal gyrus (area 22) of the non-dominant hemisphere H) It is caused by lesions of the supramarginal and angular gyri (areas 37, 39, 40) and the posterior part of the superior temporal gyrus (area 22) of the dominant hemisphere I) It is also called expressive aphasia J) It is also called receptive aphasia 218. The following statements regarding aphasia are TRUE: A) Broca’s aphasia is also called sensory or receptive aphasia B) Wernicke’s aphasia is also called sensory or receptive aphasia C) Patients with Broca’s aphasia have a fluent speech with unintelligible content due to frequent errors in word choice, inappropriate use of words, and the use of made-up words D) Broca’s aphasia is also called motor or expressive aphasia E) Broca’s aphasia is caused by lesions of the areas 44 and 45 of the dominant hemisphere F) Patients with Wernicke’s aphasia have a fluent speech with unintelligible content due to frequent errors in word choice, inappropriate use of words, and the use of made-up words G) Broca’s aphasia is caused by lesions of the supramarginal and angular gyri (areas 37, 39, 40) and the posterior part of the superior temporal gyrus (area 22) of the dominant hemisphere H) Wernicke’s aphasia is caused by lesions of the supramarginal and angular gyri (areas 37, 39, 40) and the posterior part of the superior temporal gyrus (area 22) of the dominant hemisphere I) Wernicke’s aphasia is also called motor or expressive aphasia J) Wernicke’s aphasia is caused by lesions of the areas 44 and 45 of the dominant hemisphere 219. The following statements regarding apraxia are TRUE: A) Constructional apraxia is a special type of spatial neglect B) Ideomotor apraxia is caused by lesions in the non-dominant parietal lobe C) Ideomotor apraxia is caused by lesions in the dominant parietal lobe D) Constructional apraxia is defined by an impossibility to perform learned motor activities E) Constructional apraxia is caused by lesions in the dominant parietal lobe F) Constructional apraxia is caused by lesions in the non-dominant parietal lobe G) Ideomotor apraxia is a special type of spatial neglect H) Testing for constructional apraxia includes placing the hands of a clock (or drawing one) I) Ideomotor apraxia is defined by an impossibility to perform learned motor activities J) Testing for ideomotor apraxia includes placing the hands of a clock (or drawing one) 220. The following statements regarding constructional apraxia are TRUE: A) It is defined by an impossibility to perform learned motor activities B) The patient is able to reproduce a geometric figure C) Tests used for this disorder include placing the hands of a clock (or drawing one) D) The patient is no longer able to use tools in relation to their body (brushing teeth, combing hair) or in relation to other aspects of the environment (using a key, hammer) E) It is characterized by the inability to summate a series of “temporal impressions” into understanding the temporal relations between the parts of a whole F) It is a special type of spatial neglect G) The patient is unable to reproduce a geometric figure H) It is characterized by the inability to summate a series of “spatial impressions” into understanding the spatial relations between the parts of a whole I) It is caused by lesions in the dominant parietal lobe J) It is caused by lesions in the non-dominant parietal lobe 221. The following statements regarding ideomotor apraxia are TRUE: A) It is a special type of spatial neglect B) The patient is no longer able to reproduce a block building or stick construction after a model C) Patients have difficulty reproducing a geometric figure D) It is defined by an impossibility to perform learned motor activities (on command or by imitation) in the absence of motor or sensory deficits E) It is caused by lesions in the non-dominant parietal lobe F) The patient is no longer able to use tools in relation to the environment (using a key to open a door, using a hammer) G) Patients have difficulty carrying out a sequence of actions H) It is caused by lesions in the dominant parietal lobe I) The patient is no longer able to place the hands of a clock (or drawing one) J) The patient is no longer able to use tools in relation to their body (brushing teeth, combing hair) 222. The following statements regarding ideomotor apraxia are FALSE: A) The patient is no longer able to use tools in relation to their body (brushing teeth, combing hair) B) The patient is no longer able to place the hands of a clock (or drawing one) C) The patient is no longer able to reproduce a block building or stick construction after a model D) Patients have difficulty reproducing a geometric figure E) The patient is no longer able to use tools in relation to the environment (using a key to open a door, using a hammer) F) It is caused by lesions in the dominant parietal lobe G) It is caused by lesions in the non-dominant parietal lobe H) Patients have difficulty carrying out a sequence of actions I) It is defined by an impossibility to perform learned motor activities (on command or by imitation) in the absence of motor or sensory deficits J) It is a special type of spatial neglect 223. The following statements regarding constructional apraxia are FALSE: A) It is defined by an impossibility to perform learned motor activities B) The patient is unable to reproduce a geometric figure C) It is characterized by the inability to summate a series of “temporal impressions” into understanding the temporal relations between the parts of a whole D) It is a special type of spatial neglect E) It is characterized by the inability to summate a series of “spatial impressions” into understanding the spatial relations between the parts of a whole F) The patient is able to reproduce a geometric figure G) It is caused by lesions in the dominant parietal lobe H) Tests used for this disorder include placing the hands of a clock (or drawing one) I) The patient is no longer able to use tools in relation to their body (brushing teeth, combing hair) or in relation to other aspects of the environment (using a key, hammer) J) It is caused by lesions in the non-dominant parietal lobe 224. Complete occlusion of the MCA causes stroke with: A) Cortical blindness. B) Oculogyric deviation in the direction of the affected hemisphere (centre of conjugate eye movements in the frontal lobe); C) Ipsilateral hemiplegia and facial weakness; D) Aphasia (lesions of the non-dominant hemisphere); E) Hemianopsia. F) Sensory hemisyndrome and neglect syndrome (parietal lobe - severe if non-dominant hemisphere is affected); G) Aphasia (lesions of the dominant hemisphere); H) Contralateral hemiplegia and facial weakness; I) Oculogyric deviation in the direction of the unaffected hemisphere; J) Sensory hemisyndrome and neglect syndromes (parietal lobe - severe if dominant hemisphere is affected); 225. Lateral bulbar syndrome (Wallenberg): A) Caused by thromboembolism in the posteroinferior cerebellar artery (PICA) or its branches, vertebral artery thromboembolism or dissection. B) It is a very rare trunk syndrome; C) It is manifested by chronic vertigo; D) Caused by thromboembolism in the anterosuperior cerebellar artery. E) It is manifested by cerebellar signs; F) Also called Horner syndrome; G) It is a common trunk syndrome; H) It is manifested by acute vertigo; I) It is frequently asymptomatic; J) It is a vascular syndrome; 226. Carotid artery dissection shows: A) Ipsilateral Horner's syndrome due to sympathetic plexus compression around the carotid artery; B) Contralateral Horner syndrome due to sympathetic plexus compression around the carotid artery; C) Pain is always absent; D) Embolic infarction in the territory of the anterior circulation. E) Lower cranial nerve damage (X, XII are the most obvious clinically); F) Temporo-parietal pain; G) Laterocervical pain; H) Facial pain; I) Embolic infarction in the posterior circulation territory. J) Lower cranial nerve damage cannot be clinically observed; 227. The clinical manifestation of stroke syndrome in the bilateral paramedian thalamic and midbrain territory is: A) Ophthalmoplegia; B) Coma or disturbed vigilance; C) Absence of coordination disorders; D) Not manifested by disturbed vigilance; E) Memory impairment F) Thalamic pain. G) Absence of oculomotor disorders; H) Ataxia; I) Absence of memory disorders; J) Motor aphasia. 228. Stroke in the internal capsule is clinically manifested by: A) Brachial or crural monoplegia; B) Unequal neurological deficit represented in the face, upper limb and lower limb; C) Neurological deficit equally represented in the face, upper limb and lower limb; D) No dysphasia or other cortical deficits. E) Sensorimotor loss; F) No word articulation disorder; G) Motor or sensory loss; H) Frequent aphasia or other cortical signs. I) Possible profound dysarthria from involvement of cortico-bulbar fibres; J) Sensory-motor paraplegia; 229. About brain stem infarction we can say: A) The damage to the medial lemniscus and the spino-thalamic tract is manifested by sensory disturbances; B) Nucleus V nerve entrapment is manifested by facial hypoesthesia; C) Seizure of nerve nucleus VII is manifested by facial hypoesthesia. D) Corticospinal tract damage is manifested by sensory disturbances; E) Nucleus V nerve entrapment manifested by facial paresis; F) Damage to the medial lemniscus and spino-thalamic tract is manifested by motor disorders; G) Corticospinal tract damage is manifested by hemiparesis/tetraparesis; H) Damage to the oculomotor system manifested by hemianopsia; I) Seizure of nerve nucleus VII is manifested by facial paresis. J) The damage to the oculomotor system is manifested by dilpopia; 230. About brain stem infarction we can say: A) Impairment of the reticular formation may result in altered consciousness or coma B) Vestibular connection damage is manifested by dysphagia/dysarthria C) Entrapment of IX, X nerve nuclei may manifest as nystagmus and vertigo D) Horner's syndrome results from entrapment of parasympathetic fibres E) Damage to brainstem connections and cerebellar connections manifest as dysarthria, ataxia, hiccups/vomiting F) Vestibular connections are affected by nystagmus and vertigo G) Horner's syndrome results from entrapment of sympathetic fibres H) Reticular formation damage does not affect consciousness I) Seizure of the nuclei of nerves IX, X may manifest itself by dysphagia/dysarthria J) Damage to brainstem connections and cerebellar connections manifests as aphasia, agnosia or apraxia 231. Lacunar infarction: A) Lacunae are always detectable on CT; B) Lacunae are visible on MRI or postmortem; C) Strokes without cortical involvement such as pure motor hemiparesis, pure sensory hemisyndrome, unilateral sudden onset ataxia and sudden onset dysarthria with disabled hand are typical lacunar syndromes. D) Lacunar infarcts are frequently asymptomatic; E) Lacunar infarcts are small infarcts (1.5 cm³; J) Strokes without cortical involvement such as pure motor hemiparesis, pure sensory hemisyndrome, sudden onset unilateral ataxia and sudden onset dysarthria with disabled hand are atypical lacunar syndromes. 232. About stroke investigations we can say: A) Carotid Doppler ultrasonography is performed in patients with stroke in the posterior territory who are eligible for surgery. B) CBC and blood glucose are not mandatory at presentation; C) Routine blood tests such as CBC, blood sedimentation rate, blood glucose, and clotting studies and lipids are performed within 48-72 hours; D) Cranial MRI is routinely performed within 1 hour of presentation; E) Echocardiography is performed within 24 hours to detect atrial fibrillation; F) The ideal cranial CT is performed within 1 hour of presentation; G) CBCand blood glucose ideally within 1 hour of presentation; H) Routine blood tests such as CBC, blood sedimentation rate, blood glucose, clotting studies and lipids are performed within 24 hours; I) Electrocardiography is performed within 24 hours to detect arterial fibrillation; J) Carotid Doppler ultrasonography is performed in patients with stroke in the anterior territory who are eligible for surgery. 233. Regarding neuroimaging we can state: A) CT detects brain bleedings immediately; B) Doppler ultrasonography is essential in the first 24 hours to identify severe symptomatic stenosis requiring surgery; C) CT angiography and MRI angiography are not necessary to identify arterial dissections and cerebral venous sinus thrombosis; D) Catheter angiography is often necessary in ischemic stroke. E) Stroke is often not detected in the acute phase, or only subtle changes are visible; F) Doppler ultrasonography is not essential in the first 24 hours to identify severe symptomatic stenosis requiring surgery; G) Angio CT and Angio MRI evaluation are used to identify arterial dissections and cerebral venous sinus thrombosis; H) Catheter angiography is rarely needed in ischemic stroke. I) CT does not detect cerebral hemorrhage immediately; J) Cerebral infarction is often detected in the acute phase; 234. In patients with stroke without an identified cause the following additional investigations may be required: A) Echocardiography (transesophageal echocardiography should be considered); B) Brain CT with dissection protocol; C) Screening for thrombophilia. D) Abdominal ultrasound; E) Lower limb venous Doppler echo. F) CT angiography or MRI angiography; G) Prolonged cardiac monitoring for paroxysmal atrial fibrillation; H) CT or MRI evaluation with contrast material; I) Prolonged cardiac monitoring for permanent atrial fibrillation; J) Brain MRI with dissection protocol; 235. With regard to MRI we can state: A) MRI evaluation is essential in all patients and even in cases where the cause is clear. B) Demyelinating lesions that may mimic a stroke are always evident on CT; C) MRI assessment highlights the extent and location of the infarct and illustrates clinically silent simultaneous infarcts suggesting an embolic source; D) CT evaluation is more sensitive than MRI for early infarct changes and small infarcts; E) Demyelinating lesions that may mimic a stroke can be highlighted on MRI; F) MRI assessment can help identify the underlying cause, e.g. arterial dissection using special sequences showing the false lumen (crescent sign); G) MRI evaluation is essential in young patients or in cases where the cause is unclear. H) MRI evaluation is more sensitive than CT for early infarct changes and small infarcts; I) MRI evaluation can help identify the underlying cause, e.g. arterial dissection using special sequences showing the true lumen (crescent sign); J) CT assessment highlights infarct extension and location and illustrates clinically silent simultaneous infarcts suggesting an embolic source; 236. Regarding the clinical syndrome in stroke we can state: A) Stroke in the territory of the left middle cerebral artery is manifested by left hemiparesis predominantly faciobrachial; B) Stroke in the superficial territory of the middle cerebral artery of the dominant hemisphere, not manifested by aphasia; C) Stroke in the territory of the right middle cerebral artery is never manifested by visual and sensory neglect; D) Stroke in the territory of the left middle cerebral artery is manifested by aphasia; E) Stroke in the territory of the left middle cerebral artery is manifested by right hemiparesis predominantly faciobrachial; F) Stroke in the right middle cerebral artery territory is never manifested by disability denial. G) Stroke in the territory of the right middle cerebral artery is manifested by left hemiparesis predominantly faciobrachial; H) Stroke in the right middle cerebral artery territory is manifested by disability denial. I) Stroke in the right middle cerebral artery territory is manifested by visual and sensory neglect; J) Stroke in the territory of the right middle cerebral artery is manifested by right hemiparesis predominantly faciobrachial; 237. Regarding the necessary cardiological investigations post stroke we can state: A) Identification of the cardioembolic source, primarily atrial fibrillation, can be done by ECG or ECG monitoring for 24 hours; B) Identification of the atherothrombotic source, primarily atrial fibrillation, can be done by echocardiography; C) Existence of mural thrombus requires echocardiographic evaluation; D) PFO requires electrocardiographic evaluation. E) Valvular disease requires transthoracic echocardiography; F) Transthoracic echocardiography is not necessary to identify valvular pathologies; G) PFO requires echocardiographic evaluation. H) In a significant minority of patients with stroke of unknown cause implantable loop recorder evaluation has revealed the presence of permanent atrial fibrillation; I) In a significant minority of patients with stroke of unknown cause implantable loop recorder evaluation has revealed the presence of paroxysmal atrial fibrillation; J) The presence of a mural thrombus requires electrocardiographic evaluation; 238. With regard to the FAST summary examination we can state: A) Constitutional facial asymmetry ; B) Absence of speech difficulties; C) Paramedics and the general population are encouraged to diagnose stroke based on history and a brief examination. D) Time of onset is irrelevant; E) Duration since onset of symptoms; F) Asymmetry of the face appeared suddenly; G) Sudden weakness and numbness of one or two limbs; H) Speech difficulties/dysarthria/aphasia; I) Weakness and numbness with onset of at least 7 days in one or two limbs; J) FAST summary examination can only be carried out by specialised medical professionals. 239. Regarding the stroke treatment scheme we can state: A) CT examination should always be available, it will indicate infarction and rarely reveal bleeding; B) In cerebral infarction 300 mg/day aspirin is administered if thrombolytic therapy is contraindicated; C) If thrombolysis is indicated, immediate brain imaging is necessary; D) If the CT scan shows bleedings, treatment that interferes with clotting will not be administered and neurosurgery may occasionally be necessary. E) CT examination should always be available, it will indicate bleeding, other pathologies or sometimes infarction; F) If the CT scan excludes bleedings, thrombolytic therapy is administered immediately; G) If the CT scan shows bleeding, thrombolytic therapy is administered immediately; H) If thrombolysis is indicated, immediate brain imaging is not necessary; I) If the CT examination excludes bleeding do not administer treatment to interfere with coagulation. J) In cerebral infarction 150 mg/day aspirin is given if thrombolytic therapy is contraindicated; 240. During admission to a multidisciplinary stroke unit: A) Investigation of cause and risk factors; B) Initiate thromboembolism prophylaxis; C) Swallowing assessment is not necessary; D) Swallowing assessment; E) Treating medical complications, e.g. infection, hyperglycaemia, atrial fibrillation; F) Initiation of prophylactic antibiotic therapy; G) Initiation of secondary prevention measures. H) Initiation of primary preventive measures. I) Investigation of cause and rare risk factors; J) Treatment of surgical complications; 241. Regarding stroke treatment we can state: A) In a recent meta-analysis of five studies, the benefit of endovascular thrombectomy in patients with acute ischemic stroke caused by proximal occlusion of the anterior circulation was shown. B) Approximately 25% of patients are potential candidates for thrombolysis, most are excluded due to late presentation; C) In a recent meta-analysis of five studies, the benefit of endovascular thrombectomy in patients with chronic ischemic stroke caused by proximal occlusion of the anterior circulation was shown. D) Thrombolysis insignificantly increases the chances of having minimal or no disability after ischemic stroke; E) Thrombolysis significantly increases the chances of having minimal or no disability after an ischemic stroke by reducing the area of cerebral infarction; F) Endovascular treatment is rarely performed with a retriever stent; G) Early treatment within 8.5 hours significantly increases the chance of a favorable prognosis; H) Early treatment within 4.5 hours significantly increases the chance of a favorable prognosis; I) Endovascular treatment is usually performed with a retriever stent; J) Approximately 10% of patients are potential candidates for thrombolysis, most are excluded due to late presentation; 242. Regarding stroke treatment we can state: A) Cerebral venous or sinus venous thrombosis causing ischemic stroke is not treated with anticoagulants; B) For arterial dissection, the risk of recurrent ischemic embolic stroke at the site of origin of the dissection is relatively insignificant to justify immediate anticoagulation or antiplatelet therapy; C) Cerebral venous or sinus venous thrombosis causing ischemic stroke is also treated with anticoagulants; D) Anti-aggregants are initiated for cardioembolic ischemic stroke associated with atrial fibrillation usually after 2 weeks of stroke onset; E) The disadvantage of direct oral anticoagulants compared to Warfarin is that they have a narrower therapeutic spectrum with a higher bleeding rate. F) The advantage of direct oral anticoagulants over Warfarin is that they have a broader therapeutic spectrum with a lower bleeding rate. G) For arterial dissection, the risk of recurrent ischemic embolic stroke at the site of origin of the dissection is considered high enough to justify immediate anticoagulation or antiplatelet therapy; H) High doses of aspirin (300 mg) are given immediately after thrombolysis; I) Anticoagulants are initiated for cardioembolic ischemic stroke associated with atrial fibrillation usually 2 weeks after stroke onset; J) High doses of aspirin (300 mg) are administered 24 hours after thrombolysis; 243. Exclusion criteria for thrombolysis in acute ischemic stroke: A) Symptoms suggestive of subarachnoid haemorrhage, even if CT examination is normal; B) Symptoms suggestive of subarachnoid haemorrhage and necessarily evident on CT examination; C) Epileptic seizure at stroke onset, if residual deficit is due to postictal phenomena; D) Neurological deficit recovered after an epileptic seizure; E) Persistent systolic blood pressure > 185, diastolic > 110 mmHg, or requiring aggressive blood pressure control therapy; F) Major and persistent neurological signs; G) Systolic blood pressure 2.8 mmol/L; D) INR > 1.7 if patient is on warfarin; E) Platelets > 100,000/mm³; F) INR < 1.7 if patient is on warfarin; G) Blood glucose < 26.2 mmol/L; H) Low partial thromboplastin time if patient is on heparin treatment. I) Serum glucose > 26.2 mmol/L; J) Increased partial thromboplastin time if patient is on heparin treatment. 246. Exclusion criteria for thrombolysis in acute ischemic stroke: A) Sustained severe hypertension requires treatment after 24-48 hours; B) Target for total cholesterol being below 6 mmol/L (low density lipoprotein < 3 mmol/L). C) Sustained severe hypertension requires treatment after 72 hours; D) Transient hypertension, rarely seen after stroke, usually does not require treatment as long as diastolic blood pressure does not exceed 90 mmHg; E) Statins should be given to all patients unless contraindicated; F) Statins are given to all patients on a compulsory basis; G) Blood pressure should be lowered slowly to avoid sudden drops in cerebral perfusion; H) Blood pressure should be lowered abruptly; I) Target for total cholesterol being below 4 mmol/L (low density lipoprotein < 2 mmol/L). J) Transient hypertension, often seen after a stroke, usually does not require treatment as long as the diastolic blood pressure does not exceed 100 mmHg; 247. Carotid stenosis surgery and stenting involves: A) For patients with moderate asymptomatic stenosis (50-69%), there is a minor benefit from the procedure compared to the stroke risk associated with the procedure per se which is about 3%; B) For patients with moderate symptomatic stenosis (50-69%), there is a modest benefit from the procedure compared to the risk of stroke associated with the procedure per se which is about 3%; C) Patients with 70-99% stenosis have a major reduction in 10-year stroke risk and moderate stenosis should not be treated conservatively; D) Carotid occlusion is rarely treated conservatively (no risk of distal embolization). E) Asymptomatic carotid stenoses are associated with a significant risk of recurrent ischemic stroke in the weeks immediately following a TIA or stroke; F) Carotid endarterectomy should be performed within the first 2 weeks in patients with 70-99% stenosis on the affected side if the initial ischemic stroke was not severely disabling; G) Carotid endarterectomy should be performed within the first few days of detection in patients with 70-99% stenosis on the affected side if the initial ischemic stroke was not severely disabling; H) Symptomatic high-grade carotid stenoses are associated with a significant risk of recurrent ischemic stroke in the weeks immediately following a TIA or stroke; I) Patients with 70-99% stenosis have a modest reduction in stroke risk at 5 years and moderate stenosis should be treated conservatively; J) Carotid occlusion is always treated conservatively (no risk of distal embolization). 248. Regarding post-stroke rehabilitation we can state: A) Physiotherapy does not play a vital role in preventing spasticity and contractures; B) Baclofen and/or botulinum toxin are 100% effective in the treatment of severe spasticity; C) Baclofen and/or botulinum toxin are sometimes useful in the treatment of severe spasticity; D) Video-assisted fluoroscopy during attempt to swallow presents a vital risk. E) Nasogastric tube feeding is recommended for all post-stroke patients; F) If swallowing is unsafe due to risk of aspiration, nasogastric tube feeding or percutaneous gastrostomy will be necessary; G) In general, speech recovery is enhanced by conversation; H) Physiotherapy is of particular value in the first weeks after stroke, for the prevention of spasticity and contractures; I) Video-assisted fluoroscopy during the swallow attempt is useful. J) Speech recovery is diminished by conversation; 249. Paraclinical investigations for a Transient ischaemic attack (TIA) do not include: A) Cervical MRI B) Prolonged electrocardiographic monitoring C) Echocardiography D) Cranio-cerebral X-ray E) Electromyography F) Holter Blood Pressure G) Blood Pressure monitoring H) Electrocardiogram I) Computed tomography angiography J) Doppler ultrasonography of the carotid arteries 250. It is not true about the transient ischemic attack(TIA): A) Stroke is usually avoided due to medical intervention B) Cardiac valvulopathies are not sources of embolism C) It can be caused by high blood pressure D) They are usually the result of microemboli, but can be produced by different mechanisms E) Cardiac thrombi rarely occur in patients with myocardial infarction or atrial fibrillation F) Frequently, subdural tumors or hematomas can cause episodes similar to a TIA G) It can be caused by: cardiac arrhythmias, orthostatic hypotension or decreased blood flow through atherosclerotic arteries H) The main sources of cerebral embolism are cardiac thrombi and atherosclerotic plaques at the level of the aortic arch and at the level of the carotid and vertebral system I) Subdural tumors or hematomas can cause episodes similar to a TIA J) Stroke is usually avoided due to cerebral autoregulation 251. It is true about the Willis polygon: A) It is not irrigated by the vertebro-basilar circulation B) It is irrigated by the two internal carotid arteries C) It is irrigated by the posterior circulation D) It is irrigated by the vertebro-basilar circulation E) It is not irrigated by the posterior circulation F) It is supplied by the anterior cerebral circulation G) It is not irrigated by the two internal carotid arteries H) It is a hemodynamically significant venous sinus I) It is irrigated by the anterior circulation J) It is not irrigated by the anterior circulation 252. To stratify the risk of a stroke after a TIA(transient ischemic attack), the score will be used: A) CHA2-DS2-VASc B) HAS-BLED C) ABCD2 is not used D) ATRIA is not used E) ABCD2 F) CHADS2 is not used G) CHA2-DS2-VASc is not used H) CHADS2 I) HAS-BLED is not used J) ATRIA 253. It is not true about cardioembolic stroke: A) Thrombosis in a dilated atrium secondary to atrial fibrillation is the rarest cause B) It is due to thrombosis in a dilated atrium secondary to atrial fibrillation C) A patent foramen ovale (FOP) did not allow passage of a thrombus fragment D) Mural thrombosis may occur in an affected or akinetic ventricular segment E) Is due to thrombosis in a dilated ventricle secondary to atrial fibrillation F) The heart is an important source of embolic material G) The heart is not an important source of embolic material H) A patent foramen ovale (FOP), which is a common condition, may occasionally allow passage of a fragment of thrombus I) Calcifications of the heart valves due to rheumatic or degenerative causes J) Pulmonary arteriovenous fistulas were not a cause of paradoxical embolism 254. The following are true about the risk of stroke, except: A) It occurs more frequently in people with vascular risk factors B) It increases with age C) 40% of survivors are independent at 6 months D) 40% of survivors are dependent at 6 months E) The death rate after stroke is 20-25% F) A quarter of cases occur before the age of 65 G) It does not occur more frequently in people with vascular risk factors: H) A quarter of the cases appear after the age of 65 I) It is a rare cause of adult disability worldwide J) Decreases with age 255. The intervention resulting in the most important reduction in the risk of stroke is: A) It is not the treatment and blood pressure monitoring B) Treatment of sleep apnea C) Effective control of diabetes D) Weight loss E) It is not the cessation of smoking F) Anticoagulation for atrial fibrillation G) It is not effective control of diabetes H) Blood pressure treatment and monitoring I) It's not weight loss J) Statin consumption, diet 256. There are risk factors whose correction is correlated with reducing the risk of ischemic stroke: A) High cholesterol B) Smoking C) Alcohol D) Hypertension E) Drug use F) Normal weight status G) Lifestyle H) Severe renal stenosis I) Pregnancy J) Ventricular fibrillation 257. It is true about the involuntary movements called "limb-shaking": A) They are part of the clinical data for the differential diagnosis in TIA(transient ischemic attack) B) They are caused by transient focal cerebral hypoperfusion C) They appear in multi-infarct dementia D) They are not determined by transient focal cerebral hyperperfusion E) They are determined by transient focal cerebral hyperperfusion F) They appear in the infarction of middle cerebral antery G) They appear in lacunar infarction H) They appear during thrombolysis I) They are pathognomonic for severe carotid stenosis J) They appear within aTIA(transient ischemic attack) 258. The main regions of extracranial artery stenosis are, with the exception of: A) Internal carotid artery B) It is not represented by the basilar artery C) Cerebellar artery D) Middle cerebral artery E) Posterior cerebral artery F) Anterior cerebral artery G) Basilar artery H) Subclavian artery I) Vertebral artery J) Common carotid artery 259. Regarding hypoperfusion as the cause of a stroke: A) The territories irrigated by the middle cerebral artery are particularly vulnerable B) The cerebellar artery is particularly vulnerable C) It cannot be produced in the presence of a severe stenosis in the proximal segment of the carotid arteries D) In the case of a cardiac arrest, it does not lead to stroke in the border areas between different vascular territories E) The posterior cerebral artery is particularly vulnerable F) The parieto-occipital region is particularly vulnerable G) The territories irrigated by the anterior cerebral artery are particularly vulnerable H) It can occur if there is a severe stenosis in the proximal segment of the carotid arteries I) Severe hypertension, for example in the case of a cardiac arrest, leads to infarctions in the border areas between different vascular territories J) In case of a cardiac arrest, it leads to stroke in the border areas between different vascular territories 260. Among the risk factors and rarer causes of stroke are: A) Oral contraceptives containing a small dose of estrogen increase the risk in combination with hypotension and smoking B) Thrombocythemia C) Anticardiolipin antibodies and lupus anticoagulant D) Oral contraceptives containing low dose estrogen do not significantly increase the risk of stroke, only probably in cases where they are associated with other risk factors, e.g. uncontrolled hypertension and smoking E) Vasculitis F) Thrombocytopenia G) Atrial fibrillation H) Amyloidosis I) Oral contraceptives containing a high dose of estrogen increase the risk in combination with hypotension and smoking J) Oral contraceptives that contain a high dose of estrogen do not significantly increase the risk 261. Regarding the prognosis of patients who have suffered a TIA(transient ischemic attack), a pathology that appears after 5 years is represented by: A) Hemorrhagic stroke B) Myocardial infarction C) Ischemic stroke D) Epilepsy E) It is not represented by vascular cognitive disorder F) It is not represented by myocardial infarction G) It is not represented by deep venous thrombosis H) Deep venous thtombosis I) Vascular cognitive disorder J) It is not represented by hypnotic disorders 262. In the case of a TIA(transient ischemic attack) we may have clinical evidence of a source of embolism, such as: A) Recent myocardial infarction B) Ventricular fibrillation C) It is not represented by endomyocardial fibrosis D) Rheumatic disease E) Deep vein thrombosis F) Endomyocardial fibrosis G) Carotid murmur (stenosis) H) Calcified plaque I) Valvular heart disease/endocarditis J) Atrial fibrillation or other arrhythmias 263. Regarding CADASIL: A) It is a frequent cause of ischemic stroke B) It is a rare hereditary cause of ischemic stroke C) It is an autosomal dominant cerebral arteriopathy D) It presents subcortical infarcts and leukoencephalopathy E) It is an autosomal recessive cerebral arteriopathy F) It is a rare cause of hemorrhagic stroke G) It is defined only by cortical infarcts H) It is a rare hereditary cause of dementia I) The acronym comes from cerebral dominant arteriopathy with subcortical infarcts and leukoencephalopathy J) It is a common cause of dementia 264. It is true about the arterial dissections associated with a stroke: A) They can be caused by osteopathic manipulations, hair washing in a hair salon or physical exercises B) It cannot be determined by a sudden twisting movement of the neck associated with extension (.,whiplash") C) It never presents itself as a pain in the neck D) They cannot be caused by osteopathic manipulations, hair washing in a hair salon or physical exercises. E) Most dissections affect large cervical extracranial vessels F) Sometimes they are the consequence of a trivial cervical trauma or a hyperextension movement G) Pain in the neck and face is often the key to diagnosis H) It can be caused by a sudden twisting movement of the neck associated with extension ("whiplash"). I) They cannot be caused by a simple cervical trauma J) Most dissections affect large intracranial vessels 265. Regarding the transient ischemic attack(TIA): A) It does not cause a stroke B) It determines a cerebral infarction C) It usually lasts a few seconds or minutes, with full recovery D) It can manifest as limb weakness, aphasia or vision loss E) It is a very prolonged episode of neurological dysfunction due to focal temporary cerebral or retinal ischemia F) TIA cannot predict ischemic stroke G) It usually lasts a few days, with full recovery H) It is a brief episode of neurological dysfunction due to focal temporary cerebral or retinal ischemia I) TIA can predict ischemic stroke J) It usually lasts a few seconds or minutes, with partial recovery 266. Regarding the pathophysiology of stroke: A) Arterial disease and atherosclerosis are the main pathological processes that cause stroke B) The underlying pathology responsible for stroke is not infarction or hemorrhage C) The underlying pathology responsible for stroke is infarction or hemorrhage D) The non-Caucasian population tends to have more frequent intracranial stenoses, while the white population has more frequent extracranial involvement (which correlates with coronary and peripheral vascular co-morbidities) E) Hemorrhagic cerebrovascular accident represents the largest share F) The non-Caucasian population tends to have more frequent extracranial stenoses, while the white population has more frequent intracranial involvement (which correlates with coronary and peripheral vascular co-morbidities) G) The most frequent site of formation of atheroma plaques was not in the arterial bifurcation regions H) The largest share is represented by ischemic stroke I) The most common site of formation of atheroma plaques is in the regions of arterial bifurcation such as the origin of the great vessels in the aorta J) Cerebral infarction represents the lowest share of the total stroke 267. The main risk factors for stroke that overlap with those for atherosclerotic disease are: A) Oral contraceptives B) Diabetes C) Dyslipidemia D) Intense physical exercise E) Age F) Obesity G) Hypotension H) Smoking I) Ventricular fibrillation J) Normal weight status 268. About amaurosis fugax it is true that: A) The embolus is sometimes visible during the transient attack with the ophthalmoscope (Hollenhorst plate) B) It is not part of the clinical picture of a TIA(transient ischemic attack) C) It represents a hemorrhagic stroke D) Sometimes it is caused by the passage of an embolus through the retinal arteries E) It is not suggestive of an internal carotid artery stenosis F) It is a transient, sudden loss of vision in both eyes G) It is frequently the first clinical evidence of internal carotid artery stenosis H) It is part of the clinical picture of a TIA(transient ischemic attack) I) It is a transient, sudden loss of vision in one eye J) It is a permanent loss of vision in one eye 269. With regarding intracerebralhaemorrhage, one can make the following statements: A) A large haematoma may cause herniation of the brain B) A large haematoma can’t determine brain displacement and herniation C) It is associated with a higher mortality than ischaemic stroke (up to 50%) D) It is associated with a lower mortality than ischaemic stroke E) Intracerebralhaemorrhage causes approximately 10% of strokes F) Intracerebral hemorrhages that occur in patients with chronic hypertension are not at the level of the basal ganglia G) Intracerebralhaemorrhage causes approximately 30% of strokes H) A large haematoma may act as a space-occupying lesion I) Hypertension can’t be the aetiology J) Cerebral amyloid angiopathy may be a possible aetiology 270. Regarding intracerebralhaemorrhage, the following statements are true: A) Important complication of hypertension in cerebral pathology may be: the rupture of microaneurysms and degeneration of small, deep, penetrating arteries B) Cocaine cannot cause intracerebralhaemorrhage C) Vasopressor drugs may cause haemorrhage D) Such haemorrhage is mild, with minimal clinical manifestations E) Charcot–Bouchard aneurysms are between 0.8–1.0 cm in diameter F) Charcot–Bouchard aneurysms are between 0.8–1.0mm in diameter G) Alcohol is not a risk factor H) Such haemorrhageoccurs in chronic hypertension and has well-defined sites: basal ganglia, pons, cerebellum and subcortical white matter. I) Alcohol is not a risk factor because it does not affect coagulation and platelet function J) Such haemorrhage is usually massive, often fatal, and occurs in chronic hypertension 271. Regarding cerebral amyloid angiopathy (CAA), one can make the following statements: A) It represents deposition of amyloid-β in the walls of small and medium-sized arteries in normotensive patients B) It causes lobar intracerebralhaemorrhage (especially posterior, i.e. occipital/parietal lobes) C) CAA may not cause TIA-like, transient neurological symptoms D) It is more common at ages over 60 E) Cerebral microbleeds are not usually seen on MRI sequences sensitive to haemosiderin deposition F) It is not recurrent G) CAA is not a possibleaethiology for intracerebralhaemorrhage H) It is more common in patients with Alzheimer’s disease I) CAA is associated with particular apolipoprotein E genotypes (E2) J) It represents deposition of amyloid-β in the walls of medium and large-sized arteries 272. In relation to the secondary causes of intracerebral haemorrhage, one can make the following statements: A) Secondary causes of intracerebral hemorrhage can be arteriovenous malformations, cavernomas, dural venous thrombosis and carotid artery stenosis B) Coagulopathies may cause haemorrhage C) Arteriovenous malformations, cavernomas, aneurysms and dural venous thrombosis cause around 80% of intracerebralhaemorrhages D) Haemorrhagic transformation of a large ischaemic infarct never manifests as haemorrhage E) Thrombolysis may not cause haemorrhage F) Coagulopathies may not cause haemorrhage G) Haemorrhagic transformation of a large ischaemic infarct may sometimes present as a haemorrhage H) Dural venous thrombosis may cause intracerebralhaemorrhages I) Arteriovenous malformations, cavernomas, aneurysms and dural venous thrombosis cause around 20% of intracerebralhaemorrhages J) Anticoagulants may cause haemorrhage 273. Regarding subarachnoid haemorrhage, one can make the following statements: A) Thesaccular (berry) aneurysms accounts for 70% of the causes B) In 15% of cases no arterial lesion is found C) Among the rare associations (5cm) E) The role of surgical decompression for non-cerebellar bleeds is less clear-cut F) The role of surgical decompression for non-cerebellar bleeds is well defined G) Urgent neurosurgical clot evacuation is lifesaving (and is required where the haematoma is >3cm or the patient is drowsy or deteriorating) H) Emergency neurosurgical evacuation of the haematoma is rarely important I) Placement of an external ventricular drain is needed with extension of the haemorrhage into the ventricular system J) Emergency neurosurgical evacuation of the hematoma is not recommended, regardless of the size of the haematoma 277. Regarding subarachnoid haemorrhage (SAH), one can make the following statements: A) Subarachnoid haemorrhage (SAH) means spontaneous arterial bleeding into the subarachnoid space B) A very common cause of SAH is coagulation disorders C) SAH accounts for some 25% of strokes D) It has an annual incidence of 6 per 100000 E) Arteriovenous malformations accounts for 30% of SAH F) It is unusual to find any contributing disease for SAH G) Saccular aneurysms that accounts for 70% of the causes develop within the circle of Willis and adjacent arteries H) SAH accounts for some 5% of strokes I) Subarachnoid haemorrhage does not have a dramatic onset, as such it is not easy to recognize J) Subarachnoid haemorrhage (SAH) means spontaneous arterial bleeding into the brain tissue 278. Regardingsaccular (berry) aneurysms, one can make the following statements: A) May emerge between posterior communicating and internal carotid artery – posterior communicating artery aneurysm B) Common sites are at arterial junctions C) Saccular aneurysms are an incidental finding in 1% of autopsies and can be multiple D) A common site may be at the trifurcation or a bifurcation of the middle cerebellar artery E) Saccular aneurysms develop within the circle of Willis and adjacent arteries F) An enlarging unruptured posterior cerebral artery aneurysm is the most common cause of a painful IIIrd nerve palsy G) Saccular aneurysms can’t cause symptoms by direct pressure on surrounding structures H) Other aneurysms sites can’t be on the basilar, posterior inferior cerebellar, intracavernous internal carotid and ophthalmic arteries I) A common site may be between anterior communicating and anterior cerebral artery – anterior communicating and anterior cerebral artery aneurysm J) Saccular aneurysms may cause slowly progressive symptoms, when there is usually no preceding history 279. Regarding arteriovenous malformation (AVM), the following statements are true: A) Arteriovenous malformation (AVM) often with a fistula between arterial and venous systems, causing high flow through the AVM and high-pressure arterialization of draining veins B) The risk of a first haemorrhage in unruptured AVMs (arteriovenous malformations) is approximately 2–3% per year C) Once an AVM has caused a haemorrhage, the risk of rebleeds is increased to approximately 30% per year D) AVMs can’t be ablated with endovascular treatment (catheter injection of glue into the nidus, usually), microsurgery or stereotactic radiotherapy E) 30% of AVMs are fatal and 50% with permanent disability F) Only the neurosurgeon will make a therapeutic decision regarding AVMs, the multidisciplinary approach not being necessary G) There is a clear consensus on the best treatment modality or, indeed, whether the considerable risk of intervention is lower than with a conservative approach H) An AVM (arteriovenous malformation) usually is diagnosed after a seizure, often focal in onset I) An AVM (arteriovenous malformation) usually presents following a spontaneous intracerebralhaemorrhage J) Arteriovenous malformation (AVM) is a vascular developmental malformation 280. Regarding cavernous haemangiomas (cavernomas), the following statements are true: A) Cavernous haemangiomas (cavernomas) consist of a tangle of low-pressure dilated vessels without a major feeding artery B) Surgical resection of cavernomas is often necessary C) Cavernous hemangiomas are usually symptomatic and they are not detected by imaging D) Small haemorrhages may occur but are usually lowpressure bleeds and rarely cause severe deficits E) Cavernous haemangiomas (cavernomas) have a prevalence of 0.1– 0.5% F) Cavernous haemangiomas (cavernomas) are very rare G) Multiple cavernomas often have a genetic basis H) Cavernomas may cause seizures I) Cavernous haemangiomas (cavernomas) are usually symptomatic J) Surgical resection is not required for cavernomas that gradually increase in size or that cause significant neurological symptoms 281. The clinical characteristics of subarachnoid hemorrhage (SAH) are: A) The headache from subarachnoid hemorrhage is often occipital B) In subarachnoid hemorrhage, there is a very severe headache C) Death cannot occur in SAH D) The headache from subarachnoid hemorrhage has a sudden onset E) The headache from subarachnoid hemorrhage is usually followed by vomiting F) Survivors of SAH may remain drowsy for minutes G) The mean time to peak headache in SAH is 3 hours H) Major bleeds in SAH may cause few signs I) Survivors of SAH may remain comatose or drowsy for hours, days or longer J) Papilloedema is always present in SAH 282. The clinical characteristics of subarachnoid hemorrhage (SAH) are: A) SAH is a possible diagnosis in any sudden headache B) Headache in SAH is usually followed by vomiting and often by coma and death C) SAH is a possible diagnosis in any slowly progressive headache D) Survivors of SAH may remain comatose or drowsy for hours, days or longer E) Following major SAH, there is neck stiffness and a positive Kernig’s sign only if meningo-encephalitis is associated F) In SAH, papilloedema is sometimes present, with retinal and/ or subhyaloidhaemorrhage (tracking beneath the retinal hyaloid membrane) G) Approximately 37% of patients have small ‘sentinel bleeds’ in the weeks before presenting with SAH H) Following major SAH, there is neck stiffness and a positive Kernig’s sign I) The headache from SAH is usually frontal J) Headache from SAH is moderate, having an insidious onset 283. Regarding investigations in subarachnoid hemorrhage (SAH), the following statements are true: A) CT imaging is the second-line investigation for the diagnosis of SAH B) Sensitivity of CT to detect subarachnoid blood is 50% within 24 hours of onset C) Sensitivity of CT to detect subarachnoid blood is much lower after 24 hours of onset D) Subarachnoid and/or intraventricular blood is rarely seen on CT (under 5% of cases) E) Sensitivity of CT to detect subarachnoid blood is 95% within 24hours of onset F) Sensitivity of CT to detect subarachnoid blood is much higher after 24 hours of onset G) Lumbar puncture is necessary if SAH is confirmed by CT H) CT imaging is the immediate investigation in this case I) Subarachnoid and/or intraventricular blood is usually seen on CT J) CT angiography or catheter angiography to identify the aneurysm or other source of bleeding is performed in patients potentially fit for surgery 284. Regarding investigations in subarachnoid hemorrhage (SAH), the following statements are true: A) Lumbar puncture is not necessary if SAH is confirmed by CT B) Visual inspection of supernatant CSF is usually insufficiently reliable for diagnosis C) Lumbar puncture is necessary if SAH is confirmed by CT D) Spectrophotometry to estimate bilirubin in the CSF released from lysed cells is not used to define SAH with certainty E) Paraclinical investigations always detect bleeding sources or aneurysms when there is a clear diagnosis of SAH F) Lumbar puncture should be performed if there are doubts on imaging in the case of SAH G) Visual inspection of supernatant CSF is usually sufficiently reliable for diagnosis H) In some, no aneurysm or source of bleeding is found, despite a definite SAH I) CSF becomes yellow (xanthochromic) within 12hours of SAH J) CT angiography or catheter angiography to identify the aneurysm or other source of bleeding is not performed in patients, even if they have an indication for surgery 285. Regarding differential diagnosis in subarachnoid hemorrhage (SAH), the following statements are true: A) The syndrome of reversible cerebral vasoconstriction (Call–Fleming’s syndrome) has an insidious, slowly progressive headache B) SAH occurs frequently at the onset of acute bacterial meningitis C) Thunderclap headache is used to describe only SAH D) This is sometimes difficult but a short time to maximal headache intensity and the presence of neck stiffness usually indicate SAH E) Acute bacterial meningitis can frequently cause a very abrupt headache, when a meningeal microabscess ruptures F) The syndrome of reversible cerebral vasoconstriction is named Call–Fleming’s syndrome G) The differential diagnosis of SAH with migraine is sometimes difficult H) A short time to maximal headache intensity and the presence of neck stiffness usually indicate migraine I) SAH must be differentiated from migraine J) Thunderclap headache is used (confusingly) to describe either SAH or a sudden (benign) headache for which no cause is ever found 286. Regarding complications in subarachnoid hemorrhage (SAH), the following statements are true: A) Arterial spasm, which is a complication of SAH is visible on angiography, being a cause of coma or hemiparesis B) Hydrocephalus may cause deteriorating consciousness following SAH. C) Blood in the subarachnoid space can lead to obstructive hydrocephalus D) Obstructive hydrocephalus is never asymptomatic E) Obstructive hydrocephalus, which is a complications of SAH is visible on CT (computer tomography) F) Obstructive hydrocephalus is not visible on CT (computer tomography) G) Arterial spasm is a mild complication of SAH H) In obstructive hydrocephalus, shunting is useless I) Shunting may be necessary in hydrocephalus J) The presence of arterial spasm in SAH indicates a good prognosis 287. Regarding the treatment in subarachnoid hemorrhage (SAH), the following statements are true: A) Nimodipine, a calcium-channel blocker given for 3weeks, reduces mortality B) Failure to diagnose SAH – for example, mistaking SAH for migraine – contributes to this mortality C) Only a small percentage,