Neurology and Psychiatry Lectures Notes 2022-2023 PDF

Depar tmentofneur ologyandpsychi atr y Facult yofMedi ci ne Universi tyofAl exandr ia 2022-2023  To our great late professors...

Depar tmentofneur ologyandpsychi atr y Facult yofMedi ci ne Universi tyofAl exandr ia 2022-2023  To our great late professors Prof. Omar El Garem Prof. Salah Mansour Prof. Mohammed El Fatatry Prof. Seham Rashed Prof. Ayman Ezz Eldeen Prof. Soliman Tahoun 1 |Page  Preface “Whenever a doctor cannot do good, he must be kept from doing harm.” Hippocrates. “The brain is the organ of destiny. It holds within its humming mechanism secrets that will determine the future of the human race.” Wilder Penfield The brain with its complex functional, anatomically, and physiological aspects provides a unique bridging between the two specialties of neurology and psychiatry. Since the start of the 21 century the emergence of a psychiatric st emphasis on molecular biology, neurochemistry and neuroimaging as well as the increasing consciousness by neurologists of psychiatric co-morbidities is most neurological disorders, opening to realization of co-dependence of those two specialties more than any other specialties in the medicine. It was always a dream and repeated request from our students to have a simplified book covering the undergraduate curriculum of neuropsychiatry. Now, this dream is becoming a reality and we present this fourth edition of “Alexandria Neuropsychiatry lecture notes”. Our aim is to provide a clear, simplified and up to date knowledge of clinical neurology and psychiatry integrating with it the basic neuroscience. Hope this knowledge will help our students to provide a better care for patients. Editors Staff members of neuropsychiatry department 2 |Page  With very special thanks to Ass. Prof. Hany Eldeeb Who dedicated a great deal of effort for this version of the book to be released in its best possible form. 3 |Page List of contents INTRODUCTION TO NEUROLOGY CLINICAL GUIDE 7 NEUROLOGY SHEET 8 LOCALIZATION IN NEUROLOGY 39 CLINICAL APPROACH TO “ISCHEMIC CEREBROVASCULAR STROKE“ 51 CLINICAL APPROACH TO “HEMORRHAGIC CEREBROVASCULAR STROKE“ 68 CLINICAL APPROACH TO: “EPILEPSY AND STATUS EPILEPTICUS” 76 CLINICAL APPROACH TO “HEMIPLEGIA” 91 CLINICAL APPROACH TO “PARAPLEGIA” 98 CLINICAL APPROACH TO “HEADACHE” 110 CLINICAL APPROACH TO “MULTIPLE SCLEROSIS” 122 CLINICAL APPROACH TO “COMA” 131 CLINICAL APPROACH TO “MOVEMENT DISORDERS” 151 CLINICAL APPROACH TO “CNS INFECTIONS” 167 CLINICAL APPROACH TO “NEUROPATHIES, MYOPATHIES AND NEUROMUSCULAR JUNCTION DISORDERS” 179 CLINICAL APPROACH TO “CRANIAL NERVES DISORDERS” 197 CLINICAL APPROACH TO “CERVICAL AND LOW BACK PAIN“ 208 CLINICAL APPROACH TO “ATAXIA” 220 PSYCHIATRIC SYMPTOMATOLOGY, ASSESSMENT & 225 TREATMENT PLAN 225 MYTHS ABOUT PSYCHIATRY 240 ANXIETY AND RELATED DISORDERS 248 CLINICAL APPROACH TO “MOOD DISORDERS” 258 SOMATIC SYMPTOM & RELATED DISORDERS 273 CHILD PSYCHIATRY 285 CLINICAL APPROACH TO “SCHIZOPHRENIA 294 4 |Page DEMENTIA AND DELIRIUM 312 SUBSTANCE-RELATED DISORDERS 327 EMERGENCY PSYCHIATRIC MEDICINE 338 TREATMENT IN PSYCHIATRY (PSYCHOPHARMACOLOGY) 346 DEVICES IN PSYCHIATRY 353 CLINICAL APPROACH TO “PSYCHOTHERAPY” 364 5 |Page  I. Neurology 6 |Page  Introduction to neurology clinical guide Clinical interview is a type of problem solving. We will try in our guide to help you analyze the commonly seen neurological cases that you may face in your practice and how to solve them in a simple way to make neurological interview an interesting mission. First, we should know that to be a good neurologist, you must be a good listener. You should by the end of the interview answer these two questions: What is the lesion? (A matter of history) This can be reached by perfect history taking. Analyzing the onset, course and associated symptoms of each complaint will help you decide the nature of the problem (e.g., vascular, inflammatory, neoplastic, etc.) Where is the lesion? (A matter of examination) This is the role of neurological examination to catch the localizing signs that help you define the exact site of the problem (e.g., pyramidal tract, cerebellum, spinal cord, etc.) If you could not reach the proper diagnosis by the clinical steps, you should know the art of choosing the proper investigation that may help you solve the case. How can we approach a neurological case? To answer this question, let us have 4 examples to start with: Case A → A 64-year-old man developed all of a sudden right sided weakness and mouth deviation to the left side. His past medical history is positive for diabetes and hypertension. He is known to be smoker. Case B → A 55-year-old lady presented to you with a 4-month history of gradually developing right sided weakness that progressed to complete paralysis. 7 |Page Case C → A young adult man was completely normal till he received a hit to his head and lost his consciousness. After emergency measures, he regained his consciousness with evident right sided weakness. Case D → a 32-year-old lady was completely normal till 2 days ago when she started to be feverish with headache and blurred vision. Her consciousness became clouded on the next day and by examination there was a right sided lag. These four cases were presented with the same clinical picture (i.e.m right hemiparesis) and proper history taking guided us to differentiate between 4 different causes of hemiparesis and this is the answer to the first question “what is the lesion?” The art of localization is the way of collecting the clinical signs to answer the second question “where is the lesion?”. It will be discussed in a specific section. Finally, remember that neurological interview is not a problem as long as we approach it in a simple and systematic way to reach the diagnosis. Neurology Sheet History Personal data Name: for identification, communication, registration. Sex: some diseases affect particularly one sex more than the other, or x- linked (e.g., Duchenne muscle dystrophy). Age: certain disorders are seen in certain ages e.g.; cerebral atherosclerosis usually doesn’t occur before middle age. Occupation: this might expose the patient to trauma or intoxication, as when a porter suffers from sciatica due to lumbar disc protrusion 8 |Page  Residency: A disease may be endemic in certain localities, as leprosy in certain areas of upper Egypt Marital status Date of admission Complaint The patient is asked to mention his present complaints and the duration of each. One must write down the words used by the patient and not their scientific (technical terms), e.g., when he says fainting attacks, you must not use syncope instead of fainting. They are arranged chronologically. A. Motor symptoms (+ involuntary movement) ▪ Wasting: loss of muscle bulk ▪ Weakness ▪ Cramps: painful muscle contraction ▪ Involuntary movement: myoclonus, chorea, convulsions B. Sensory symptoms ▪ Paresthesia: Abnormal sensory perception ▪ Allodynia: perceiving non-painful stimuli as painful ▪ Hyperalgesia: exaggerated pain sensation ▪ Hypothesia: diminished pain sensation ▪ Anesthesia: loss of pain sensation C. Cranial and bulbar symptoms (+ special senses) ▪ OCULAR: Diplopia, Ptosis – ▪ Visual: e.g., Loss of vision - Dimness of vision ▪ Facial asymmetry 9 |Page  ▪ Difficulty in deglutition (dysphagia) – chocking attacks – difficulty in speech (dysarthria) – abnormal voice (dysphonia) D. Visceral symptoms Urinary Commonly neurologic: 1. URGE (UMN bladder-release stage): involuntary urinary voiding due to detrusor over activity (usually before reaching the bathroom to perform voluntary voiding). Occurs in release from spinal shock or UMN lesion. Also called overactive bladder. 2. OVERFLOW incontinence (LMN bladder or UMN bladder shock stage): - involuntary urinary voiding due to increased intravesical pressure secondary to urinary retention. Occurs in shock stage of UMN lesion. Also called underactive bladder. Commonly non-neurologic: 1. STRESS incontinence: - involuntary urinary voiding due to increased intraabdominal pressure. Occurs mainly due to gynecologic causes (vaginal/uterine prolapse). 2. Hesitancy: difficulty in initiating micturition (it can be caused by either neurological or non-neurological causes) N.B: Urgency is the intense desire for urinary voiding without incontinence. It shares the same causes of urge incontinence + it can occur in urinary tract irritation (non-neurologic). Fecal : constipation – incontinence Impotence E. Manifestations of increased intracranial pressure manifestation: headache, vomiting and blurring of vision 10 | P a g e  F. Ataxia (imbalance). G. High cortical function Loss of skilled movements (apraxia) – Aphasia - Alternation of consciousness Present history (The story of each complain should make sense) Each complain should be analyzed: Onset course extent Associated symptom. Treatment received, response to therapy. Negative data After that the examiner might find it necessary to ask certain questions to make the onset and course of the disease very clear (natural history). ❖ Onset: sudden (within seconds to minutes) acute (within minutes to hours) subacute (days) gradual or chronic (weeks to months) It is also important to ask about symptoms such as fever, loss of weight, alteration of consciousness, convulsions, headache, vomiting, giddiness, disturbance of vision. ❖ Course: Progressive Regressive 11 | P a g e  Remission & relapse It is also important to ask about symptoms such as fever, loss of weight, alteration of consciousness, convulsions, headache, vomiting, giddiness, disturbance of vision. ❖ Important negative data must be mentioned. ❖ Therapies and response to treatment Past history Similar condition. Chronic medical illness: DM, HTN+ treatment (controlled or not) Any previous illness or trauma (particularly to the head and spine), however mild, has to be mentioned. Drugs. Allergy. If the patient had any specific infection (as syphilis, tuberculosis, bilharzias), he should be asked whether he received the proper treatment or not. Family history Similar condition in the family with detailed relation of relative and age at onset +/- natural history Relevant neurological condition Consanguinity It is important since some nervous diseases are hereditary (as hereditary ataxia), some run in families (as hypertension and diabetes) and some infections are present in family members (as TB and leprosy). Personal (social) history 12 | P a g e  Lifestyle, work, stress. Inquiry into the habits of the patient, alcohol intake or substance abuse e.g. hashish, benzodiazepines, heroin, etc.. The diet of the patient should be asked about, particularly if there is a possibility of nutritional deficiency. Sleep habits. To answer the question of the pathology of the lesion, a good history is able to do so in most of the cases even before carrying out the clinical examination. Psychogenic (e.g., hysterical hemiplegia), the diagnosis has to be arrived at from two angles; the positive angle (psychological stress), and the negative angle (no signs of organic disease). Organic lesion: o Congenital (hereditary- error of development -intrauterine infection) o Acquired: we lay stress on the onset and course of the disease Sudden onset (within seconds to minutes) and regressive course: hemorrhagic, embolic, traumatic Acute onset (within minutes to hours) and regressive course: thrombotic stroke, acute inflammation. Subacute onset (days) and regressive course: immune mediated, metabolic Gradual onset or chronic (weeks to months) and progressive course: malignancy, neurodegenerative disease, chronic inflammation. 13 | P a g e  Remission & relapse: demyelination – vasculitis Stair-case curve: cumulative effect of multiple minor vascular events example cerebral atherosclerosis Examination Instruments used: Hammer Tuning fork 128 Pen light Cotton piece Coffee smell Disposable pins or toothpicks Items to be fulfilled: 1. PHYSICAL DEVELOPMENT& GENERAL APPEARANCE 2. MENTAL STATUS 3. SPEECH & ARTICULATION 4. CRANIAL NERVES.MOTOR EXAM 5. GAIT & COORDINATION 6. REFLEXES 7. SENSORY SYSTEM 8. TROPHIC & VASOMOTOR CHANGES 9..SKULL & SPINE EXAINATION 10. SPECIAL TESTS 11. GENERAL EXAMINATION A. General appearance and behavior Physical development will indicate any gross endocrinal or nutritional disturbance e.g., height, weight. 14 | P a g e  General appearance may be very helpful for early diagnosis, as the expressionless face of parkinsonism syndrome which may be evident before the appearance of the disease. Pallor, jaundice etc. B. Mental state examination 1) State of consciousness Glasgow coma scale is the standard and should be assessed in every patient. [See coma lecture]. 2) Intellectual functions I. Orientation person place time II. Attention & concentration. - Ask the patient to subtract serial 7s from 100. - Ask the patient to name five things that start with a particular letter. - Ask the patient to rename days of week backward. III. Memory ✓ Remote memory: ask about childhood data, important events known to have occurred when the patient was younger or free of illness. ✓ Recent memory: the past few days what the patient had for breakfast, lunch, dinner. ✓ Immediate retention or recall: digit span measures; ability to repeat six figures after examiner; ability to repeat three words immediately. IV. Intelligence: mathematical problem 3) Affect & emotion. i. Experience ii. Expression 15 | P a g e Neurological disorders with emotional lability: Pseudobulbar palsy Multiple sclerosis Chorea C. Speech & articulation ✓ Disturbance of speech is called, according to its severity, dysphasia or aphasia. ✓ Disturbance of articulation is called dysarthria, or anarthria. Speech 1..Spontaneous speech a. Informal interview: Attention should paid to the fluency of speech, presence of initiation difficulty, the presence of word-finding pauses. b. Structured task 2. Naming objects: tested by asking the patient to name objects, object parts, pictures, colors, or body parts to confrontation. 3. Repetition: Repetition of words and phrases should be deliberately tested. 4. Reading 5. Writing Simplified examination: Receptive: 16 | P a g e  ✓ Auditory: Give the patient orders to do: start with one order then 2 orders, then 3 integrated complex orders ✓ Visual: Give the patients the same orders written on the paper and tell him to do it. Expressive Naming objects ✓ Spoken. ✓ Written. Types of aphasia or dysphasia: Expressive aphasia (=motor=Boca’s aphasia) Receptive aphasia (=sensory =Wernicke’s aphasia) Global aphasia: no reception & no expression Nominal aphasia: cannot name objects. Alexia: cannot read Agraphia: cannot write. Articulation: Read (alfatiha) !‫الفاتحة‬ Repeating a long word with multiple syllables: ‫إسكندرية‬ Count from1-100 Dysarthria means only faulty articulation of speech sounds. It may result from central lesions of the brain or cerebellum, intoxications (such as alcohol), or neuromuscular disorders. Examiner should pay attention to different form of dysarthria for example slurred speech which occurs with lesions along the course of the pyramidal tract, staccato or scanning speech which occurs in cerebellar lesion, low monotonous tone or nasal tone of voice etc. D. Cranial nerves examination 17 | P a g e I. Olfactory nerve Ask the patient to close his eyes. Test each nostril separately. Hold a non-irritant odour in front of the open nostril and ask the patient to sniff. Wait a moment for the patient to perceive the odor and then identify it. NB: Avoid the use of irritating substances as ammonia which will stimulate the trigeminal nerve. The most frequent causes of anosmia are the common cold, COVID, allergic rhinitis, smoking, and head trauma. Hyposmia also occurs in, Wernicke-Korsakoff syndrome, Kallman syndrome, Alzheimer’s disease, Parkinson’s disease and lesions of the olfactory bulbs and tracts like meningeal neoplasms- classically, olfactory groove meningiomas- that compress the olfactory bulbs and tracts. II. Optic VISUAL ACUITY: Counting Finger-Snellen Chart VISUAL FIELDS: by the confrontation method Take a distance of 1 meter between the doctor & patients. Then check the field from the periphery, from the 4 directions. FUNDOSCOPIC EXAM: Optic disc - Optic cup – Retinal vessels 18 | P a g e III Oculomotor, IV Trochlear, VI Abducens 1. Palpebral fissures: detect any dropping of the upper eye lid (ptosis), or retraction of it. Also, observe the position of the eyes for any exophthalmos (proptosis) or enophthalmos. Detect any nystagmus in the position of rest. Looking to the examiner’s handheld at the level of the palpebral fissure (straight ahead gaze), normally the upper eye lid covers 1/5th of the cornea. 2. Pupils: observe the size, equality of the two pupils, shape or regularity, and mobility or reaction both to light (direct and consensual) and to accommodation. 3. Ocular movements: these are tested both for horizontal and vertical movements, and for convergence. Observe any limitation of movement in any direction and any squint and diplopia. Also observe any nystagmus, which may be apparent only on conjugate ocular (gaze)deviation. V. Trigeminal 19 | P a g e A. Motor It supplies the muscles of mastication (pterygoids, masseter and temporalis). The patient should clench his teeth and palpate these muscles. On opening the mouth there is deviation of the jaw to the same side of the lesion B. Sensory: ALL 3 DIVISIONS: ✓ Ophthalmic ✓ Maxillary ✓ Mandibular Compare both sides pain sensation by a disposable pin. C. Reflexes: 1) Jaw jerk (afferent& efferent are the trigeminal nerve) Response: normal absent or just elicited, if exaggerated →pseudobulbar palsy Pseudobulbar palsy: Bilateral pyramidal lesion above the level of the pons + Emotional lability 2) Corneal reflex (afferent trigeminal & efferent is the facial nerve) Response: eye closure, if absent –> abnormal VII. Facial ✓ It supplies the muscles of the face, which are used for both voluntary movements and emotional expression. ✓ Observe any asymmetry of the face (especially nasolabial folds and forehead corrugations) and any involuntary movements. ✓ Test: Movements = motor: 20 | P a g e  ✓ The upper face (closure of the eyes, elevation of the eyebrows, frowning) ✓ The lower face (showing the teeth, pursing the lips blowing and whistling) ✓ Test emotional movements by telling the patient a joke & see the degree of the deviation on laughing. Test for the autonomic function (lacrimation & salivation( Test for the taste sensation in the anterior 2/3 of the tongue: Dry the tongue & put solutions on each tongue half & see if he will identify the taste. VIII. Vestibulocochlear If there is impairment or loss of hearing, it might be of the conducting type (middle ear disease), or of the perceptive type (nerve lesion ie sensory neural hearing loss). The tuning fork (512 Hz) tests are used to distinguish one from the other. These tests are based on the fact: 1) In a normal individual air conduction for sounds is better than bone conduction. 2) In middle ear deafness air conduction is diminished or lost, while bone conduction is relatively increased. 3) In nerve deafness both air and bone conduction are diminished or lost. Two tests are used: (both are not very reliable, particularly the second) a) Rinne’s test: A vibrating tuning fork base is placed on the mastoid process (the ear being closed by the examiner’s finger), and when the patient cannot hear any more in this position, it is held with the branches close to the auditory meatus. In a normal individual, and in a patient with partial nerve deafness, the sound can be heard by air conduction after bone conduction has stopped. In middle ear deafness this does not occur. 21 | P a g e  b) Weber test: A vibrating tuning fork base is placed on the forehead in the middle line. The sound is heard in a normal individual at the middle line, in nerve deafness at the normal ear, and in middle ear deafness at the affected ear. IX. Glossopharyngeal The glossopharyngeal nerve: usually not affected alone, but with vagus nerve. A) Sensory functions: examine the taste in the posterior third of the tongue (rather difficult( B) Reflex functions: do the pharyngeal (gag) reflex (by tickling the back of the pharynx, the posterior pharyngeal wall; after depressing the tongue by a spatula. X. Vagus The vagus: is concerned with the motor functions of palate, pharynx & larynx. The palate: In unilateral paralysis, on saying , watch the uvula, it will deviate to the healthy side. In bilateral paralysis the uvula will be central, yet not elevated. There will be nasal speech and regurgitation of fluids through the nose when the patient tries to swallow. XI. Accessory The spinal accessory nerve supplies the upper part of the trapezius and sternomastoid. a) Trapezius is tested by asking the patient to shrug his shoulder, the physician should examine it from the back b) Sternomastoid is tested by asking him to rotate his chin towards the opposite side, and push against resistance> The other method to examine both sternomastoids together by pushing with the chin down on the examiner's hand. 22 | P a g e XII. Hypoglossal The hypoglossal nerve: is the motor nerve of the tongue. It is tested by asking the patient: a) To protrude his tongue and observe any deviation (which will be to the paralyzed side), wasting (by wrinkling of the mucosa), or involuntary movements (tremors, fasciculations( b) To press with the tongue against the inside of either cheek and its power is tested with your finger on the outside of the patient’s cheek. E. Motor examination 1) Posture: Fixed attitude due to the illness ▪ Flexed attitude → parkinsonism. ▪ Hemiplegic attitude ▪ Skeletal deformities e.g. High arched foot, Scoliosis, Kyphosis ▪ Examine for wrist or foot drop, by telling the patient to extend his hand / foot and move it against gravity. Causes of wrist drop: 1. Peripheral neuropathy 2. Radial nerve injury Causes of foot drop: 1.Peripheral neuropathy 2. Peroneal nerve injury 2) Involuntary movements Tremor – Chorea – Athetosis – Dystonia – Myoclonus – Tic [refer to involuntary movements lecture] Fasciculations: ✓ Inspection ✓ Inspections after tapping with a hammer. ✓ Inspection after hyperventilation. 23 | P a g e 3) Muscle status ✓ Watching the muscle bulk for any asymmetry. If in doubt measure the circumference by a meter. First choose a near fixed bony prominence, measure a distance then measure the circumference. In the other limb do the same and compare both sides. ✓ If decreased it is called atrophy, if increased it is hypertrophy Causes of atrophy: Muscle dystrophy, Peripheral neuropathy, Root lesion, AHC disease Cause of hypertrophy: Exercise Anabolic steroids Pseudohypertrophy like hypertrophy but with muscle weakness (seen in Duchenne muscle dystrophy) 4) Muscle tone The basal muscle tone is tested by a passive movement of the limb, where the examiner moves the limb across the full range of mobility of each joint (the elbow, hand & knee are the best sited to evaluate the muscle tone) The comment is: normal, hypotonia or hypertonia. Causes of hypertonia: 1) Rigidity (extrapyramidal) e.g., Parkinson's disease. ✓ Cog wheel (if tremors are present) 24 | P a g e  ✓ Lead pipe 2) Spasticity; Clasp-knife in upper motor neuron lesion e.g., stroke, MS Causes of hypotonia: Lower motor neuron lesion: e.g. Peripheral neuropathy Chorea Cerebellar lesion UMNL in shock stage 5) Muscle power ✓ We examine groups of muscles around each joint on both sides. ✓ First ask the patient to move a limb freely then perform the action against resistance. ✓ The patient is asked to do a certain action e.g. if we are examining the flexors of the elbow, we ask the patient to flex and then try to extend the elbow. We mention if there is weakness, determine its degree and if there is a certain pattern of weakness. Degree of weakness: 0= no movement at all 1 = flickers (movement too fine to move a joint) 2 = can move with elimination of gravity (parallel to the floor) 3 = can move against gravity, but not against resistance 4 = can overcome mild resistance 5 = normal power (can oppose any resistance) Patterns of weakness: Hemiparesis: weakness of one side of the body 25 | P a g e  Paraparesis: weakness of both lower limbs Quadriparesis: cervical cord lesion, bilateral pyramidal lesions Monoparesis: weakness of one limb Proximal vs distal weakness Weakness of pyramidal distribution: o Upper limb; extensor more than flexors o Lower limb; flexors more than extensors F. Coordination Testing the cerebellar function In the Upper limb ✓ Finger to finger test: ask the patient to touch the tip of the index finger of both sides, [once with the eyes opened, then with the eyes closed] ✓ Finger to nose test: ask the patient to touch the tip of his nose with the index finger; [once with the eyes opened, then with the eyes closed] ✓ Finger to the examiner finger: touch with the tip of the index the doctor’s fingertip. ✓ Rapid alternating movements: Ask the patient to rapidly supinate and pronate the hand. Dysdiadokokinesia = having difficulty in rapid alternating movement 26 | P a g e ✓ Rebound phenomena: o Tap on outstretched patient’s upper limbs. o Sudden release of the examiner’s resistance of the patient’s firmly flexed forearm (while protecting the patient's face) In the Lower limb ✓ Heel Knee Chin test: o Three steps; ask the patient to do the followings: ▪ Elevate the lower limb of the examined side in extension. ▪ Point with the heel of the examined side to the knee of the opposite one. 27 | P a g e  ▪ Pass the heel on the chin of the tibia in a straight line. ✓ Tandem walk: Ask the patient to walk in a straight line with one foot immediately in front of the other (heel to toe), Stay close enough to patient to catch them if he falls. Romberg Test The patient stands barefoot with his feet close to each other. First, eyes open then close the eyes. If okay with eyes open, but sways or falls with his eyes closed = +ve Romberg’s [Mainly tests deep sensation]. G. Gait Ask the patient to walk and watch his gait. Abnormal neurological gait patterns: Stamping: in deep sensory loss 28 | P a g e  Waddling: in proximal muscle weakness, hip dislocation Circumduction /Hemi paretic: in pyramidal tract lesions Shuffling: in parkinsonism High steppage: in foot drop Spastic (if advanced scissoring): bilateral Pyramidal lesions Ataxic: in cerebellar lesions H. Reflexes: 1) Deep tendon reflexes Generally, expose and relax the limb, tap on the tendon and observe the muscle contraction. A good reflex = good limb positioning + localizing the tendon + good hammer tapping +/- asking for reinforcement when needed. Biceps; C 5,6 Brachioradialis; C 5,6 Triceps; C 6,7 Knee L3,4 29 | P a g e  Ankle S1,2 Reinforcement technique ✓ Upper extremities: clench teeth ✓ Lower extremities: clench the teeth or lock fingers and pull one against the other. Clonus A repetitive contraction in response to sudden sustained contraction. Patellar clonus: suddenly push the patella downwards in an extended limb. If positive the patella will move upwards and downwards Ankle clonus: flex the knee and ankle, then suddenly contract the foot; If positive the foot will repeatedly flex and extends. 30 | P a g e  Causes of hyperreflexia: Anxiety Pyramidal lesion above the center of the reflex thyrotoxicosis Causes of hyporeflexia / areflexia: Congenital areflexia Upper motor neuron lesion in shock stage Lower motor neuron lesions: AHC, root lesions, Grades ofpolyneuropathy, reflexes Hypothyroidism Grade zero: absent after reinforcement. Grade 0+: present after reinforcement Grade 1: just elicited. Grade 2: brisk Grade 3: exaggerated. Grade 4: exaggerated with clonus. B) Superficial reflexes Abdominal reflex: o Upper abdomen T7- T10, o Lower abdomen T 10 - T12 Strike the relaxed abdomen (with the knees slightly flexed) from outside inwards, quickly and compare both sides. 31 | P a g e Normal response → present If absent this means an upper motor neuron lesion on this side Plantar reflex S1 ▪ With a key strike the outer side of the foot from the heel upward towards the toes. ▪ Normally the big toe will flex. ▪ If it extends =dorsiflex +/- fanning of other toes, this is positive Babinski’s sign. Causes of an extensor plantar (Babinski sign): 1. Pyramidal tract lesion 2. Normal in babies < 12 months 3. In deep coma 4. During seizures and postictal. 32 | P a g e  C) Visceral reflexes: Vesical reflex: controlling the urinary flow &bladder. Genital reflex: ask about potency. Anal Reflex: controlling defecation and anal sphincter. D) Pathological reflexes Glabellar reflex Wattenberg reflex Finger jerk reflex Hoffman reflex I. Sensory system examination 1) Superficial sensation Sensory examination starts from distal to proximal and check the three sensory modalities. Start also from the pathological side to the normal side. a) Pain ✓ It's a must to use a disposable pin in pain sensation (tooth pick can do the job). ✓ prick the patient skin in an area with normal sensation (check the face as you know from the previous examination if it is normal or not) ✓ If the patients say that the pain sensation is less than the other point proceed till you reach the area with normal sensation. ✓ Based on history and examination done till now, will direct the sensory examination pattern. e.g., looking for sensory level, glove and stocking hypothesia, radicular sensory loss. etc. 33 | P a g e  ✓ Pain is carried by the lateral spinothalamic tract. b) Touch ✓ The same procedure but using a brush or cotton piece. ✓ The pathway carrying this sensation is mainly the spinothalamic tract. c) Temperature: ✓ Use 2 different objects, with different temperature, follow the same pattern of examination as in pain sensation. ✓ Temperature is carried by the spinothalamic tract. 2) Deep sensation ✓ We start usually in the lower limb before the upper limb. ✓ We need to discriminate between deep sensory loss secondary to peripheral neuropathy or due to posterior column affection. a) Vibration sense ✓ The main goal of this type of examination is to differentiate between polyneuropathy and sensory affection due to cord lesion. o Use a 128 Hz tuning fork, o Tap it till it vibrates, o Then put it on the medial malleolus till the patients says that he cannot feel the vibration. o Then move it to the anterior superior iliac spine and ask the patient if he still feels it or not, if not proceed to the clavicle ✓ It can be tested in the back over the spine to detect a level. ✓ Compare both sides. ✓ The vibration sense is usually the first deep sensation to be lost. b) Joint position & movement ✓ fix a proximal phalanx and move the inter-phalangeal joint move it to make the patient feel the movement and show him the directions to be examined (upwards/ downwards) then tell the patient to close his eyes. 34 | P a g e  ✓ Ask him if his distal phalanx / big toe is moving or not (joint movement); and then ask him where the tip is (joint position). c) Pressure sense ✓ press a muscle gently and ask the patient if he can feel the pressure and check for tenderness on pressure. 35 | P a g e 3) Cortical sensation a) Point localization. Ask the patient to close his eyes, and apply a pin prick or touch him, and ask the patient where was the stimulus. b) Two Point Discrimination Touch the patient's body in two places simultaneously.& Check if he can identify that these are 2 stimuli. Alternate irregularly with one-point touch.and ask the patient to identify "one" or "two stimuli”. c) Graphesthesia With the blunt end of a pen or pencil, draw a large number or letter on the patient's palm or sole, ask the patient to identify the number. If the patient is illiterate, ask him if you are drawing a line or circle on his skin. d) Stereognosis Place a familiar object in the patient's hand (coin, paper clip, pencil, etc.) and ask the patient to tell you what it is.and check on both sides. Patterns of sensory loss: Glove and stalking hypothesia: peripheral neuropathy Radicular sensory loss denoting: root lesion Sensory or motor loss in a confined area in: Individual nerve lesions Multiple sensory loss in different anatomically distant sited: Mononeuritis multiplex If one limb is involved: Plexus lesions. Sensory level: Spinal cord lesions 36 | P a g e  Hemi-hypothesia without involvement of the face: Cervical hemi-section of the cord. Hemi-hypothesia with involvement of the face; internal capsule. J. Skull & spine examination Micro/macrocephaly, Hydrocephalus Examination of the spines for: Tenderness - Deformity (scoliosis/kyphosis) K. Trophic Changes: ✓ Like loss of skin appendages, like hair & nails ✓ Ulcers or loss of the tips of fingers; polyneuropathy L. Other systems: Chest examination: for sarcoidosis, TB, malignancy. Cardiac examination: for rheumatic or ischemic heart. disease, arrhythmia. Abdominal examination: for liver diseases, organomegaly. Patterns of affection: Focal lesion: (one lesion can explain all signs) e.g., vascular, traumatic, tumors. Multifocal lesion: disseminated in several sites, not anatomically related e.g., Multiple sclerosis, vasculitis, metastases, syphilis. Diffuse systemic lesions: in anatomically related system, e.g., Hereditary ataxia, motor neuron disease, B12 deficiency. Site of the lesion UMNL ✓ cortical 37 | P a g e  ✓ Subcortical; white matter ✓ internal capsule ✓ brain stem ✓ spinal LMNL ✓ Anterior horn cell ✓ Root: motor or sensory ✓ Peripheral nerve ✓ Neuromuscular junction and muscle 38 | P a g e  Localization in neurology What is meant by localization? It is our ability to figure out the exact site in the nervous system affected in each neurological disorder according to specific neurological signs Basic anatomical background The central nervous system is divided into central and peripheral parts. The central part consists of the brain and spinal cord. The brain is divided into: two cerebral hemispheres, two cerebellar hemispheres and centrally located brain stem ( bulb) that is divided into three parts: midbrain, pons and medulla oblongata. The Cerebral Cortex is the grey matter of the brain. It is divided into 4 lobes: 1. Frontal lobe Prefrontal cortex: The expanse of cortex anterior to the motor and pre- motor areas subserves executive functions. Patients with frontal lobe damage may have difficulty using information not immediately at hand to direct behavior. They therefore exhibit poor planning and judgement (see below). The motor cortex (pre-central gyrus, area 4). It contains the pyramidal cells that are the first part of the motor descending tract (corticospinal or pyramidal). Each motor cortex supplies the contralateral side of the body in an inverted pattern (i.e. the head area is present caudally and the lower limb area is present cranially ) 2. Parietal lobe The somatosensory cortex (post-central gyrus, areas 3,1 and 2). 3. Occipital lobe 39 | P a g e  The visual cortex (calcarine cortex, occipital lobes, area 17) the visual pathways: retina optic nerve optic chiasm optic tract lateral geniculate body optic radiations visual cortex). 4. Temporal lobe The auditory cortex (Superior temporal gyrus). Cerebral dominance The two cerebral hemispheres are not functionally equivalent. The following functional asymmetries have been well-documented: Language In right-handers, the left hemisphere is dominant for language. In left-handers, either left hemisphere dominance or bilateral language capabilities are the commonest findings. Handedness Handedness reflects a functional hemispheric asymmetry for fine motor ability. The Basal Ganglia The basal ganglia are a group of anatomically closely related subcortical grey matter nuclei. Damage to these nuclei does not cause weakness, but can cause dramatic motor abnormalities (e.g., rigidity and involuntary movements) 40 | P a g e The Diencephalon Diencephalon consists of the thalamus, hypothalamus, subthalamus, and epithalamus. The subthalamus is considered with the basal ganglia. The thalamus This complex structure serves to process all sensory input (except olfactory) coming from the contralateral side of the body to the cortex, Somatosensory input from both the posterior column/medial lemniscus system for position and vibration and the spinothalamic system for pain and temperature relay in the thalamus. Lesions affecting this part of the thalamus can therefore cause loss of all sensation on one side of the body.it also has some influence on motor (via input from basal ganglia and cerebellum) and cognitive function. The hypothalamus The hypothalamus exerts control over the pituitary gland and thus over endocrine function in general, and it has extensive connections with brainstem autonomic nuclei. Lesions of the hypothalamus affect appetite, emotional behavior, temperature control, and numerous other autonomic and endocrine-influenced behaviors. The Brain Stem and Cerebellum 41 | P a g e Brain stem contains three central structures that contain all the ascending and descending tracts.it contains also the cranial nerve nuclei as follows: - Midbrain: Oculomotor and trochlear nerves - Pons: Trigeminal, abducent, facial and vestibulocochlear nerves - Medulla: Glossopharyngeal, vagus, accessory and hypoglossal nerves. The cerebellum consists of two hemispheres on each side of the brain stem. Lesions of one cerebellar cortex result in ataxia on the same side as the lesion. The main functions of the cerebellum are coordination of motor movement, balance and sharing in tone regulation. The Spinal Cord The spinal cord is the simplest portion of the central nervous system, with the same general structure at every segmental level. The spinal cord is divided into 8 cervical, 12 thoracic (dorsal), 5 lumbar and 5 sacral segments. Each segment of the spinal cord is divided into central H shaped grey matter parts including both motor and sensory nuclei and a peripheral white matter containing both ascending and descending tracts. Each segment has two roots (a dorsal sensory and a ventral motor) that unite at each segment giving a pair of spinal nerve roots ( one on each side) that are considered the first part of the peripheral nervous 42 | P a g e system that involves nerve roots, plexuses, peripheral nerves, neuromuscular junction or muscle. The plexuses are responsible for supplying both upper and lower limbs. They consist of union of some spinal nerves for each limb. The brachial plexus consists of the roots of cervical nerves (C5, C6, C, C8) and first thoracic segment and is responsible for the nerve supply of the upper limb, while the lumbosacral plexus consists of the roots of lumbar segments (L2, L3, L4, L5) and sacral segments (S1, S2). The thoracic roots do not unite to male plexuses. They come directly from the spinal cord to supply the corresponding parts of the trunk. Motor (descending) pathway It is divided into upper and lower motor neuron tracts: 43 | P a g e The upper motor neuron is responsible for the motor function of the contralateral side of the body. It consists of The corticospinal (pyramidal) tract that starts from the pyramidal cells of the motor cortex and descends in a white matter bundle (corona radiata) that collects in a small white matter structure deeply seated in the hemisphere ( internal capsule) then descends on the same side of the brain stem till the lower part of the medulla where it decussate ( cross) to the opposite side to descend in the spinal cord where each segment receives its corresponding fibers that ends just at the anterior horn cell where the lower motor neuron starts by the motor roots → plexuses→ peripheral nerves→ neuromuscular junction → muscles. 44 | P a g e The motor functions of the head and neck are performed by the corticobulbar (corticonuclear) tracts that start from the head area of the motor cortex of the contralateral hemisphere and descends in the same pathway of the corona radiate and internal capsule till they reach the corresponding part of the brain 45 | P a g e stem in which the cranial nucleus lies. Thereby, the upper motor neuron crosses the midline to the opposite side where it ends in the corresponding cranial nucleus. Thereby, the lower motor neuron tract of the cranial nerve starts to supply the specific part of each cranial nerve. Sensory (ascending) pathway Sensory input from the body can be divided according to the location of its receptors into: - Superficial sensation (receptors are in the skin): includes pain, touch and temperature. It is carried through spinothalamic tracts. - Deep sensation (receptors are in the deep structures): includes vibration and joint sensation. It is carried through the dorsal column. All types of sensations are carried from the body through the sensory nerves. Once they enter the spinal cord through the dorsal root ganglion, they are divided into two different tracts. Deep sensation from one side of the body is carried on the dorsal (posterior) column that ascends on the SAME side of the spinal cord till it reaches the upper part of the pons where it decussates to the contralateral thalamus where it relays. Thereby, the second order neuron starts from the thalamus through the sensory radiation to end in the sensory cortex in the parietal lobe in which the body is represented anatomically in an upside-down pattern. Superficial sensation takes the same peripheral way till the dorsal root ganglion of each corresponding segments where it decussates and ascends in the OPPOSITE side of the spinal cord in the spinothalamic tracts till the contralateral thalamus where it takes the same pathway of deep sensation. 46 | P a g e By the end of this section, we will try to answer our question where is the lesion i.e., how can you localize the lesion? The answer will be given when you examine your patient and figure out the sum of the neurological signs found and put them under the perfect anatomical site, either sensory or motor and if motor is it an upper or a lower motor neuron lesion. This can be achieved by checking the different parts of sensory and motor examination. Upper motor neuron lesions UMNL versus lower motor neuron lesions LMNL: Upper motor neuron lesions include any lesion that may affect either any part of the corticospinal or corticobulbar tracts (starting from the cerebral cortex down to 47 | P a g e the spinal cord just before the anterior horn cell or the brain stem just before the cranial nerve nucleus, respectively). Lower motor neuron lesions of the cranial nerves include any lesion affecting either the cranial nerve nucleus, cranial nerve itself or the muscles supplied, while those of spinal nerves include any lesion in the anterior horn cell, anterior root, plexus, peripheral nerve, neuromuscular junction or muscles supplied. Both UMNL & LMNL present with weakness, but the pattern of weakness differs, and the associated signs also help to differentiate. Weakness in some lower motor neuron lesions has certain anatomical distribution that is usually bilateral and symmetrical (i.e., proximal in myopathies and distal in neuropathies) while in upper motor neuron lesion it is usually unilateral in the opposite side of the lesion and it may take a certain distribution in specific muscle groups rather than others (i.e. in the upper limbs elbow extensors are weaker than flexors and in the lower limbs the knee flexors are weaker than extensors). Associated signs may help also like: - Deep tendon reflexes: decreased or even absent in LMNL – increased in UMNL. - Plantar reflex: flexor in LMNL – extensor in UMNL. - Abdominal reflexes: preserved in LMNL – absent in UMNL. - Muscle tone: decreased in LMNL – increased in UMNL (except in shock stage). Clinical quizzes: In each of the following examples we should localize: - The type of the lesion (UMNL or LMNL) - The pattern of weakness either → 48 | P a g e  a. Monoparesis or monoplegia (partial or total weakness of one limb only, respectively) b. Hemiparesis or hemiplegia (weakness of both upper and lower limbs on one side of the body due to affection of corticospinal tract on the contralateral hemisphere or ipsilateral spinal cord above C5). c. paraparesis or paraplegia (weakness of both lower limbs due to affection of the spinal cord below T1 or both lower limb areas of the cerebral cortex. - The anatomical site of the lesion (right or left) depends on the side affected (i.e., if we say right hemiparesis, we mean the weakness of the right side of the body that is caused by a lesion in the left cerebral hemisphere, so we refer to the side of the weakness itself). - The extent of the lesion depends on the area affected (i.e., a very small lesion in the internal capsule may lead to an extensive area of weakness as the fibers are densely arranged while the same lesion in another part; cortex or corona radiate may cause a less extensive damage because the fibers are widely distributed). - Spinal cord lesions usually include a mix between motor and sensory manifestations particularly if the cord is trans-sected completely or partially → a. Complete trans-section of the cord above C5 will lead to loss of all ascending sensations from both sides of the body and loss of motor functions of the four limbs (i.e., quadriplegia). b. Hemi-section of the spinal cord above C5 will lead to loss of motor function on the same side of the lesion (i.e., spinal hemiplegia), loss of deep sensation from the same side of the lesion and loss of superficial sensation from the opposite side. c. Complete trans-section of the cord below T1 and above L2 will lead to loss of all sensations ascending from both sides of the body till the level of trans-section (i.e., sensory level) and loss of motor functions of both lower limbs (i.e., paraplegia). d. Hemi-section of the spinal cord below T1 and above L2 will lead to loss of motor function of the lower limb on the same side of the lesion (i.e. monoplegia), loss of deep sensation from the same side of the lesion and loss of superficial sensation from the opposite side up to the level of hemi-section. 49 | P a g e  Test yourself in the following quizzes and figure out the clinical finding if the brain is affected in the following sites: Left cerebral frontal cortex (the upper part) Left cerebral frontal cortex (the lower most part) Central lesion affecting the uppermost part of both cerebral cortices. Left internal capsule (including all the corticospinal fibers and the corticobulbar fibers to the facial nerve) Left midbrain (including the corticospinal fibers and the oculomotor nerve nucleus). Left pons (including the corticospinal fibers and the facial nerve nucleus). Complete trans-section of the spinal cord at C3 level. Hemi section of the right side of the spinal cord at C4 level. Complete trans-section of the spinal cord at T12 level. Hemi section of the right side of the spinal cord at L1 level. Once you perfectly answer these quizzes, keep calm and be sure that you got the clinical pearls of localization, and you are ready to start your neurology course! 50 | P a g e  Clinical approach to “Ischemic Cerebrovascular Stroke“ Case 1-1: A 68-year-old man was brought to the emergency room after suddenly developing speech difficulty and weakness of the right arm and leg. He was in his usual daily routine 2 hours ago when he was observed by family members to become mute and could not move his right side. His past medical history is significant for hypertension and angina. He is known smoker for 20 years. The patient’s temperature is 36.6°C, heart rate 84 beats/min and blood pressure 172/86 mmHg. His physical examination reveals an irregular cardiac rhythm. Neurologic examination shows an alert, attentive patient who is able to follow some simple commands but has severe impairment of word fluency, naming, and repetition. He could not express himself in words. There is a left gaze deviation and mouth deviation to the left side, but he can close his both eyes properly. There is severe weakness of the right upper extremity and, to a lesser degree, weakness of the right lower extremity. The left limbs display full antigravity power without drift for 5 seconds. Q1: What is your provisional diagnosis? Q2: How can you support your diagnosis? Q3: How will you manage this case? Case analysis: This is a common example of a case of cerebrovascular stroke, to approach such a case you should first know that most types of CVS either ischemic or hemorrhagic present themselves with a SUDDEN onset. 51 | P a g e -The most likely diagnosis in a patient with abrupt onset of focal neurologic deficits is an acute cerebrovascular event. The deficit may vary according to the arterial territory affected. Stroke, or cerebrovascular accident, is a neurological deficit of sudden onset attributable to the loss of perfusion of a portion of the brain from vascular occlusion or hemorrhage. Ischemic stroke is caused by vascular insufficiency, whereas hemorrhagic stroke is associated with a mass effect from the blood clot impinging on brain tissue. When a patient presents with weakness, numbness, or speech difficulties, a brain imaging study such as a CT or MRI is extremely valuable to distinguish between an ischemic stroke and an intracerebral hemorrhage and to help rule out a stroke mimic. In most of the cases you may not be able to differentiate clinically between ischemic and hemorrhagic stroke and for this you should support your diagnosis by brain imaging to Distinguish between an ischemic stroke and an intracerebral hemorrhage. If you did a regular CT brain it can exclude hemorrhage which appears hyper dense in CT. If CT was unremarkable, you can reach to the conclusion that it is an ischemic CVS till it can be confirmed by an MRI brain with diffusion image that is very sensitive to ischemic changes in the first hour of onset on contrary to usual CT that may remain unremarkable for ischemia up to 48 hours later. Because intervention can improve outcome in ischemic stroke, the patient should be rapidly assessed clinically and radiologically in the FIRST GOLDEN HOUR for possible thrombolytic therapy or mechanical thrombectomy. If proved to be hemorrhagic it should be treated in another way as will be mentioned later. 52 | P a g e 53 | P a g e  Cerebrovascular stroke Def.:- Stroke is defined as a clinical syndrome consisting of 'rapidly developing clinical signs of focal disturbance of cerebral function secondary to disturbance of cerebral circulation. It is caused by either reduced blood flow to the brain (ischemic stroke) or the rupture of blood vessels in the brain (hemorrhagic stroke). Types: - Cerebrovascular disorders are classified into: - ISCHEMIC (80%) which may be → o Thrombotic where an artery (either large or small vessel) is occluded by a thrombus. o Embolic where an embolus is detached (either from the heart itself or from a large artery) is detached and occludes an artery. o Cerebral hypoperfusion resulting in watershed infarction. o Venous infarction. - HEMORRHAGIC (20%) which may be → o Primary intracerebral hemorrhage (10%) (inside the brain tissue itself). o Subarachnoid hemorrhage (10%) (in the subarachnoid space around the brain tissue). Ischemic stroke 54 | P a g e Ischemic stroke: Cerebral infarction associated with mostly IRREVERSIBLE occlusion of the arteries leading to neurologic symptoms of greater than 24-hour duration. Transient ischemic attack “TIA”: A cerebral ischemic event associated with mostly REVERSIBLE occlusion of the arteries leading to reversible focal neurologic deficits lasting mostly seconds to minutes and not more than one hour and generally no evidence of cerebral infarction. Reversible ischemic neurological deficit “RIND”: A cerebral ischemic event associated with mostly REVERSIBLE occlusion of the arteries leading to reversible focal neurologic deficits lasting mostly more than one hour but not more than 24 hours and generally no evidence of cerebral infarction. Pathophysiology Within the ischemic area, there are two major zones of injury: - The core ischemic zone: where neurons start to die within minutes. Every minute in which a large vessel ischemic stroke is untreated, the average patient loses about 2 million neurons. “TIME IS BRAIN”. - The ischemic penumbra: (the term generally used to define ischemic but still viable cerebral tissue). A rim of mild to moderately ischemic tissue lying between tissue that is normally perfused and the area in which infarction is evolving, may remain viable for a few hours. However, neurons in this region will die if reperfusion is not established within a few hours. 55 | P a g e Risk factors 1) Non-modifiable risk factors: ▪ Aging: the incidence of stroke doubles for each decade after the age of 55 years. ▪ Male gender. ▪ Positive family history of stroke. ▪ Ethnic: higher incidence in blacks. ▪ Genetic. 2) Modifiable risk factors: ▪ Hypertension: It’s the most important modifiable risk factor for stroke. ▪ Diabetes Mellitus (DM): Prediabetics have also an increased risk of stroke. ▪ AF and other cardiac risk factors: AF and other cardiac arrhythmias such as paroxysmal supraventricular tachycardias without fibrillation are associated with higher stroke risk. ▪ Dyslipidemia: Increased total cholesterol and low density lipoprotein (LDL), and decreased high-density lipoprotein (HDL) levels increase the risk of ischemic stroke. This association is stronger and more evident with large artery ischemic stroke. ▪ Sedentary Behavior, Obesity and Metabolic Syndrome: Physically active individuals have lower stroke risk and stroke mortality due to the 56 | P a g e  associated reduction in the prevalence of hypertension, DM and excess body weight. ▪ Alcohol Consumption, Substance Abuse and Smoking: Heavy alcohol consumption and abuse of illicit substances; including cocaine, heroin and amphetamines increase the risk of ischemic and hemorrhagic strokes. ▪ History of a previous stroke or TIA. ▪ Drugs like oral contraceptive bills. Causes ❖ THROMBOTIC :- ✓ associated with accumulation of atherosclerotic plaques within the lumen of the artery, usually at the bifurcations. o Intracranial o Extracranial It can cause stroke by one of three mechanisms→ Embolic material from the plaques can dislodge and occlude more distal artery. Plaques can cause progressive stenosis that eventually cause complete occlusion of the artery. progressive narrowing can cause sever narrowing without occlusion of the artery leading to hypoperfusion of the brain tissue. Large artery atherosclerosis (either Intracranial or Extracranial) Small artery disease (lacunar infarct): Infarction 5 min after the maximum/last benzodiazepine dose without interval recovery, as occurs in approximately 40% of patients with convulsive status epilepticus, should prompt preparation for second-line therapy as this now represents the established status epilepticus phase. Second-line therapy Options include: intravenous fosphenytoin (20 mg/kg, maximum 1500 mg); valproate(40 mg.kg, maximum 3000 mg); and levetiracetam (60 mg.kg, maximum 4500 mg) Alternative second-line therapy includes I.V. phenobarbital (15–20 mg/kg) if not given previously. Despite its effectiveness, phenobarbital use is limited by higher frequency of sedation, respiratory depression and hypotension. ICU management: refractory and super-refractory status epilepticus Refractory status epilepticus (continuing seizure activity despite second-line therapy) occurs in 33% of status episodes, while super-refractory status epilepticus (continuous seizure activity 24 h after the induction of anesthesia) occurs in 4%. 89 | P a g e Refractory status epilepticus in a patient who is presented with or has ongoing convulsive status epilepticus should prompt ICU admission and consideration for tracheal intubation for the induction of anesthesia. Anesthetic IV doses of phenobarbital, lorazepam, or pentobarbital may be necessary in refractory cases; in such instances, intubation and O2 therapy are required to prevent hypoxemia. TREATMENT OF ANY COMPLICATIONS; METABOLIC – BLOOD GASES abnormalities. 90 | P a g e  Clinical approach to “hemiplegia” Hemiplegia is clinically defined as weakness of pyramidal distribution in the upper and lower limb. It is usually associated with different pyramidal signs and other associated symptoms that differ according to the level of affection. Typically, in hemiplegia of sudden or acute onset, the patient passes into the following two phases: ▪ Shock stage: the acute phase with flaccid paralysis and areflexia on the affected side. ▪ Spastic stage: the chronic phase with clasp knife spasticity on the affected side, exaggerated deep tendon reflexes, hemiplegic posture (upper limb elbow flexion taking the upper hand and lower limb in knee extension) and circumduction gait. The cases of chronic onset usually pass directly to the spastic phase with unnoticed shock stage. Classification of hemiplegia according to etiology: 1. Cerebrovascular Accident I. Thrombosis, Embolism or hemorrhage II. Transient Ischemic Attack 2. Head Trauma (Brain contusion, epidural hematoma) 3. Migraine 4. Todd's Paralysis (post ictal) 5. Brain Tumour a. Primary or metastatic disease 6. Infection (Brain abscess, encephalitis, Meningitis) 7. Vasculitis 91 | P a g e 8. Multiple Sclerosis 9. Perinatal injury or congenital diseases Classification of hemiplegia according to etiology: Vascular: sudden or acute onset – regressive Encephalitis: acute onset – fever and disturbed state of consciousness – regressive course Epilepsy (Todd’s paralysis) progression over seconds post ictal to minutes then improve. Migraine - progression over seconds to minutes then improve after headache attack. Demyelinating disease: remission and relapse OR secondary progression over days. Mass (tumor or abscess): gradual progressive - progression over weeks. Classification of hemiplegia according to localization: Cortical lesion Subcortical lesion Internal capsule Brainstem lesion Spinal cord lesion Cerebral hemiplegia The most common causes of hemiplegia with lesions in either cortical or subcortical structures. a. Cortical lesions: 92 | P a g e  - Weakness, which is more focal [only face or face & upper limb]. Generalized hemiplegia needs extensive cortical affection. - Signs of cortical dysfunction (aphasia, seizures, apraxia i.e. loss of skilled movements, headache) b. Subcortical lesions: - The weakness is still limited but more likely to produce equal weakness of the face, arm, and leg on the contralateral side. Extensive affection of corona radiata may cause focal weakness - No signs of cortical affection. Capsular hemiplegia: (Small lesions can lead to extensive deficits due to condensed fibers in the internal capsule) Characterized by Contralateral ▪ Hemiplegia (usually involves upper and lower limb equally). ▪ Hemihypothesia. ▪ Hemianopia (visual field defect). ▪ Upper Motor Neuron facial palsy (affection of lower face only). Brainstem lesions: Causing crossed hemiplegia→ a. Ipsilateral lower motor neuron cranial nerve palsy (according to the site): - Midbrain (3rd and 4th cranial nerves on the same side) -pons and cerebellopontine angle (5th – 8th) -medulla (9th – 12th). b. Contralateral hemiplegia. c. Ipsilateral ataxia (if cerebellum or one of its connections are involved. 93 | P a g e Spinal hemiplegia:(Brown Sequard syndrome) The lesion should be due to hemi-section of the spinal cord at the cervical region above C5 (the start of brachial plexus supplying upper limb). It leads to: a. Ipsilateral hemiplegia sparing the face. (Affected pyrami9dal tracts of the same side). b. Ipsilateral Loss of proprioception. (Affected dorsal column of the same side). c. Contralateral Loss of pain, temperature. (Affected crossed spinothalamic tracts of the opposite side). Pure Motor Hemiparesis It is usually produced by lacunar infarcts (obstruction of very small vessels cause small infarcts in the white matter called lacunes). The most common sites: - Basis pontis. - Posterior limb of internal capsule. Functional hemiplegia 94 | P a g e Never diagnose psychogenic before excluding all organic cause by proper clinical examination and investigations. Case “4-1” A 15-year-old right-hand dominant male became briefly unconscious after being tackled in a high school football game. He was unresponsive for approximately 30 seconds then slowly regained awareness over the following 2 minutes. He reported no neck pain but did complain of a moderate generalized headache as well as nausea and tinnitus. When tested 5 minutes after his injury he was oriented only to place and the name of his coach, did not know the month, day, or year, could not recall who was President, and had no memory of the series of plays immediately prior to becoming unconscious. His speech was quite slow and deliberate. His pupils were unequal, round, and reactive to light, and he had facial asymmetry with deviated angle to the right. Finger-to-nose testing was negative. He had evident left sided weakness with marked hypotonia and hyporeflexia on the affected side. Q1: What is the lesion? Q2: Where is the lesion? Q3: How can you support your diagnosis? Case analysis: Hemiplegia is defined as paralysis of the longitudinal half of the body. Hemiparesis is defined when the paralysis is mild just weakness not complete paralysis. It is a symptom, not a disease so its management should be directed mainly towards the underlying cause. The key in approaching a case of hemiplegia depends on proper history taking and perfect examination to determine the specific level of affection (e.g. cerebral, brain stem or cervical cord). 95 | P a g e Management of hemiplegia: Investigations should be tailored according to the suspected cause of the problem that is suspected by proper history taking. 1.Imaging is a must according to the site (CT or MRI). 2. Investigations of the cause. Lab investigations should be tailored according to the suspected cause of the problem that is suspected by proper history taking. Treatment is directed to treatment of the cause and includes some general points of care of the patient: Physiotherapy and rehabilitation. Assess deglutition and introduce a nasogastric tube in case of dysphagia to prevent aspiration and choking. Speech therapy for dysphasia is present. Treat any respiratory or urinary tract infection. Case (4-2 test yourself) A 43-year-old right-handed woman presents to the office with hearing loss, facial paralysis, and headache. Her history began one month ago with a sudden decrease in hearing in her right ear. One week prior to this visit she began to notice weakness of the right face, which has now progressed to complete paralysis. Over the last 3 months she has had intermittent right occipital headache, and clumsiness and imbalance if she turns quickly. She denies any change in her voice or difficulty with swallowing or swallowing difficulty. Her past medical history is unremarkable. Her physical examination shows an obvious right complete facial paralysis. Her extra-ocular movements are normal. There 96 | P a g e are no cerebellar signs. Left sided hemiplegia with left extensor plantar and brisky reflexes on the left side. Q1: What is the lesion? Q2: Where is the lesion? Q3: How can you support your diagnosis? 97 | P a g e  Clinical approach to “paraplegia” Definition: It is the inability to walk or stand due to weakness of both lower limbs, due to neurological problem affecting both lower limbs & sometimes the sphincters due to interruption in any part of the motor pathway from the cerebral cortex to the muscles. Impairment in motor function of the lower extremities with or without involvement of sensory system and/or sphincters ▪ Paraplegia - Complete paralysis. ▪ Para paresis - Partial paralysis. The definition excludes conditions in which movement is impossible (with inability to walk) without true muscular paralysis, such as: - Disturbed tone (hypotonia, spasticity) - Marked incoordination (sensory or cerebellar ataxia) - Severe pain (sciatica) - Musculoskeletal: MG, Mechanical causes (ankylosed joints) - Vascular as intermittent claudication - Debilitating disease and toxicity - Mental deficiency. Level of affection: ▪ CERVICAL ABOVE C5 - UMN signs and sensory loss in all 4 limbs =quadriplegia ▪ CERVICAL C5 TO T1 - LMN signs and segmental sensory loss in arms, and UMN signs in legs ▪ THORACIC CORD - Spastic paraplegia with a sensory level on trunk. 98 | P a g e  ▪ CONUS MEDULLARIS - Sensory loss in sacral area and extensor plantar response. ▪ CAUDA EQUINA - LMN signs in lower limbs + Saddle shape hypothesia PARAPLEGIA DUE TO UPPER MOTOR NEURON LESION It is due to bilateral pyramidal tract lesion, most commonly in the spinal cord (spinal paraplegia), and less commonly in the cerebral parasagittal region (cerebral paraplegia). Spinal paraplegia Causes of Spinal paraplegia a) Focal: Paraplegia with sensory level. b) Diffuse: Paraplegia in extension. c) Diffuse: Paraplegia in flexion. Causes of Focal paraplegia with sensory level i. Compression: - Vertebral: Fracture or fracture-dislocation of the vertebra, disc prolapse and spondylosis, Pott's disease, neoplastic diseases (primary or metastatic), deformity of the vertebral column as kyphoscoliosis. - Meningeal (extramedullary): Extradural e.g., leukemic deposits, dural e.g., meningioma, Intradural e.g., neurofibroma. - Cord (intramedullary): Syringomyelia. ii. Inflammatory: Transverse myelitis, Myelomeningitis, Myeloradiculitis. iii. Vascular: Anterior spinal artery occlusion. Causes of Diffuse Paraplegia Mild (partial) lesion damaging the pyramidal tract caused by A diffuse disorder affects one or more systems selectively and is usually bilateral and symmetrical. 99 | P a g e  a) Heredofamilial: - Hereditary spastic paraplegia. - Hereditary ataxias e.g., Friedreich's ataxia. b) Symptomatic: B12 deficiency (subacute combined degeneration of the spinal cord). c) Idiopathic: motor neuron disease. Paraplegia in extension Occurs in initial stages of the lesion. Partial transection of the spinal cord affecting the pyramidal tracts. Hypertonia is more evident in the extensor muscles group. Paraplegia in flexion Occurs when the disease progresses further or the is complete damage of the cord. More hypertonia in flexor group of muscles. Results in flexor posture of the limb. Clinical picture of acute spinal paraplegia A) Spinal shock ▪ Loss of voluntary movements. ▪ Loss of all sensations (sensory level). ▪ Reflexes are lost in shock stage, plantar is lost. ▪ Muscle tone: flaccid. ▪ Sphincteric function: urine retention, priapism. ▪ Autonomic: loss of sweating below the lesion, edema. B) Recovery of the reflex function: ▪ Loss of voluntary movement. ▪ Loss of all sensations below the lesion. ▪ Reflexes are exaggerated, plantar extensor. ▪ Muscle tone: spastic. 100 | P a g e  ▪ Sphincteric function: reflex micturition, defecation and erection. ▪ Autonomic: excessive sweating. Clinical picture of chronic spinal paraplegia ▪ Gradual onset of paraplegia in extension / flexion. ▪ Tone: Spastic. ▪ Power: Flexors are weaker than extensors. ▪ Muscle spasms. ▪ Reflexes: exaggerated, plantar extensor. ▪ Spinothalamic tract & post. Column affected. ▪ Sphincters: first urgency, then automatic bladder, reflex sexual response. ▪ Autonomic: reflex stimulation leads to excessive sweating. Cerebral (cortical) Paraplegia Causes in the Parasagittal Region ▪ Traumatic e.g., depressed fracture of the vault of the skull, subdural hematoma. ▪ Vascular e.g., superior sagittal sinus thrombosis. ▪ Inflammatory e.g., encephalitis, meningoencephalitis. ▪ Neoplastic e.g., parasagittal meningioma. C/P: ▪ Fits. ▪ Cortical sensory loss (no sensory level). ▪ Mental manifestations. ▪ May be aphasia. ▪ Cranial nerve palsy. Classification: 101 | P a g e Focal→ ▪ Acute: o Depressed fracture o Thrombosis of unpaired anterior cerebral artery o Thrombosis of SSS ▪ Chronic: o Parasagittal meningioma. Diffuse→ ▪ Acute: o Encephalitis o MS ▪ Chronic: o Congenital diplegia o Atherosclerosis o MS in 10% of cases PARAPLEGIA DUE TO LOWER MOTOR NEURON LESION 1. Anterior horn cells: Symptoms: Marked wasting. Fasciculations. Weakness. Hypotonia. Absent reflexes. Causes: ▪ Acute: Poliomyelitis (fever, patchy, intact sensation, asymmetrical, unilateral). ▪ Chronic: Motor neuron disease. 2. Roots: Cauda equine syndrome Symptoms: Saddle shape anesthesia or hypothesia with radicular sensory loss (L5-S2). 102 | P a g e  LMNL weakness & paralysis Sphincteric disturbance (bowel and bladder), Impotence. Absent ankle reflex (S1, S2). low back pain. Causes: ▪ Due to bony compression or disc protrusions in lumbar or sacral region. ▪ Inflammation: Radiculitis (viral, Syphilis, idiopathic) ▪ Compression: Lymphoma, hemangioma, hemangiosarcoma, neurofibroma Pott’s, disc prolapse 3. Spinal nerve plexus in the pelvis Causes ▪ Pott’s disease. ▪ Trauma. ▪ Pelvic tumors. ▪ Disc prolapse. 4. Peripheral nerve Symptoms: Glove & stoking hypothesia Absent ankle reflex Distal and symmetrical 5. Muscles Symptoms: Bilateral Symmetrical Proximal> distal muscles No fasciculations Absent tendon reflexes 103 | P a g e  No sensory loss No sphincter disturbance 6. Functional paraplegia Symptoms: Common in female. Positive angle: the onset is preceded by a psychological stress. Negative angle: on examination there is no evidence of organic disease (e.g., no extensor plantar reflex, bizarre finding as bizarre gait). No sphincteric disturbance. No wasting. Normal reflexes. Don’t diagnose functional element before you exhaust yourself to exclude organic cause. Case 5-1 A 59-year-old man presents with the complaint of low back pain over the past 6 months. 2month later, he started to have difficulty with walking that progressed to complete dependence on a wheelchair within 3 months. He became unable to hold urine. His wife reports that he could not feel the urge to urinate, and she usually finds him wet. He has been healthy all of his life and presents yearly for an annual checkup. There is no history of alcohol abuse or exposure to toxins. He admits to a 30-year smoking history. The review of systems is significant for weight loss and productive cough. His general examination is normal. Cranial nerve and sensory examination findings are unremarkable. Motor strength testing is normal except for evident weakness in both lower limbs. The deep tendon reflexes are exaggerated in both lower limbs in comparison to upper limbs with a Babinski sign present bilaterally. Sensory examination revealed diminished all sensations till the umbilicus. 104 | P a g e ◆ What is the most likely diagnosis? ◆ What is the next diagnostic step? ◆ What is the next step in therapy? Case analysis: Paraplegia is a symptom of many underlying diseases. Perfect history taking (as usual) is the key in differentiating the cause of paraplegia. In this case the gradual onset of symptoms with the progression over months directed our attention to a kind of neoplastic lesion (mostly metastatic if we respect the associated systemic complaints). Examination (that revealed a case of paraparesis with sphincter affection and sensory level) guided us to the site of the lesion (mostly dorsal spine). If the pattern of sensory affection is different (glove and stocking for example) and no sphincter affection the answer to our question where the lesion is will be peripheral nerve for sure. APPROACH TO PATIENT WITH PARAPARESIS History→ Onset: o Sudden: Trauma (e.g., fracture dislocation of vertebrae), vascular (e.g., thrombosis of ASA, endarteritis, hematomyelia). o Acute: Infection - Epidural Abscess Transverse Myelitis o Gradual: Neoplastic e.g., meningioma, ependymoma, glioma, astrocytoma. 105 | P a g e  Duration of symptom Short duration: Traumatic, infective causes. Long duration: Neoplastic, hereditary, congenital, demyelinating causes. Symptoms: ❖ Sensory: Ask about pattern of sensory loss: o Sacral sparing or sacral area involved. o Radicular (root) pain indicates an extradural lesion. o Distal symmetrical sensory loss. o Cortical sensory loss. ❖ Motor o Limb involvement: Symmetrical or asymmetrical. o Weakness: Proximal or distal muscles. o Weakness: Progressive or static. ❖ Associated symptoms. o Fever/Seizures/Delayed milestones. o Specific systemic symptoms e.g., vitamin deficiency. o Any preceding illness, specific trauma, prior vaccination, Involuntary movements. o Ask about bladder and bowel involvement. o Significant past history and family history o In younger children: ▪ Antenatal, natal, post-natal history. ▪ Maternal infection. ▪ Perinatal asphyxia. ▪ Hyperbilirubinemia. ▪ Hospitalization. Neurological examination→ ▪ Higher mental status: Affected in cerebral and degenerative diseases. 106 | P a g e ▪ Cranial nerve examination: Affected in brain stem lesions. ▪ Tone: Increased in UMN disease, decreased in LMN disease. ▪ DTR: Exaggerated in UMN lesions, absent in LMN lesions, and spinal shock. ▪ Sensory examination: To assess particular sensory level, to find the extent of sensory loss. ▪ Proper examination of skull and spine: To look for any localized tenderness, depressed fracture or deformity. ▪ Sphincter assessment to localize the site of affection. Investigations→ ▪ MRI brain/spine; most diagnostic for brain or spinal lesions MRI brain is more informative than CT. o It helps in diagnosing degenerative, neoplastic, vascular, infective lesions. ▪ Spinal MRI: Sagittal views – differentiates syringomyelia from intramedullary tumors, transverse myelitis. o It also shows cord compression whether internal or external. ▪ Plain X-ray Spine (Lateral and oblique view) ▪ CT scan of the spine ▪ EMG and nerve conduction: o For diagnosis of paraplegia due to cauda equina affection or peripheral neuropathy or myopathy ▪ Laboratory investigations: o B12 serum level. o Tumor markers. ▪ CSF examination. o To R/O infection-bacterial/tubercular/viral meningitis. o CSF culture and sensitivity testing o C.S.F electrophoresis to show oligoclonal bands of multiple sclerosis. 107 | P a g e  o Inflammatory spinal lesions [increased protein and cells]. o Spinal tumors [cytology for tumor cells]. o Guillain-Barre syndrome [increased protein with no or few cells; lymphocytes]. o Multiple sclerosis [increase protein – oligoclonal band] COMPLICATIONS OF PARAPLEGIA ▪ Bed sores ▪ Contractures ▪ Urinary tract infection ▪ Pneumonia ▪ Deep venous thrombosis TREATMENT OF PARAPLEGIA i. Treatment of the cause ii. Prevention and treatment of complications: a. Bedsores: air mattress – good skin care. b. Bowel & bladder incontinence: catheterization – treatment of urinary tract infection. c. Deep vein thrombosis: low dose heparin. d. Pneumonia: respiratory exercises – early treatment of chest infection. e. Pulmonary embolism. f. Psychiatric Complications: treat depression. g. Rehabilitation: early physiotherapy. iii. Symptomatic Treatment: a. Analgesics and sedatives for pain. b. Muscle relaxants for the spasticity. c. Vitamins and mineral supplementation. iv. Rehabilitation 108 | P a g e  a. Management of complications. b. Occupational therapy. c. Gait retaining. d. Community re- integration. Case 5-2 (test yourself) A 25-year-old female is brought into the emergency room (ER) after falling during a volleyball match. Her teammate notes that she was starting to have more difficulty with her serve. On arrival, she can no longer raise her legs and labors to adjust herself in bed. She has also begun to complain of shortness of breath. She denies fever but states that 3 weeks ago the entire team suffered from abdominal cramps and diarrhea. The patient denies previous health problems. On examination, she appears weak and slightly dyspneic. She can only keep her arms up against gravity for 10 seconds. She has evident weakness of both lower limbs with decreased sensation of pain and fine touch to her knees. Her reflexes are absent. She has no skin lesions or sphincter affection. ◆ What is the most likely diagnosis? ◆ What is the next diagnostic step? ◆ What is the next step in therapy? 109 | P a g e  Clinical approach to “headache” Definition Headache is pain that occurs in one or more areas of the head. Headache disorders are characterized by recurrent headache attacks. Epidemiology ✓ Half of the adult population have had a headache at least once within the last year. ✓ Headache disorders are the most common disorders of the nervous system. Classification of headache It is mainly classified into: 1) Primary type: in which there is NO structural or metabolic abnormality underlined. 2) Secondary type: either structural abnormality (extracranial or intracranial) or metabolic disorder. Types of primary headache 1- Migraine 2- Tension type headache 3- Cluster headache Sources of secondary headache A- Extra cranial: ✓ Acute sinusitis ✓ Eyes/orbit (e.g., error of refraction and acute glaucoma) ✓ Ears (e.g., otitis media) ✓ Teeth ✓ Blood vessels (e.g., temporal arteritis) B- Intra cranial: 110 | P a g e A-Temporal arteritis: A systemic, inflammatory, vascular syndrome that predominantly affects the temporal arteries. ✓ occurs in elderly. ✓ throbbing headache ✓ elevated ESR ✓ treated with steroids. B-Subarachnoid hemorrhage. C-Meningitis D-Tumors ✓ 50% of patients with brain tumors have headache. ✓ It is also associated with features of raised ICP (blurred vision and projectile vomiting). ✓ The headache worsens on awakening, cough, sneeze and strain. E- Metabolic disorders associated with hypoxemia, hypercapnia, and anemia, possibly related to the cerebral vasodilation that may accompany these conditions. DIAGNOSIS OF HEADACHE ▪ Because no biologic markers or diagnostic tests exist to determine headache type, history is the single most important element in the evaluation of the headache patient. ▪ Imaging is used to exclude structural causes for secondary headaches (CT is a simple rapid screening method to exclude hemorrhage as a cause of headache. If we suspect other etiologies MRI brain with contrast should be considered). Case 6-2 111 | P a g e A 59-year-old man presents with the complaint of headaches and difficulty concentrating over the past 6 weeks. He has been healthy all of his life and presents yearly for an annual checkup. He describes the headaches as occurring primarily over the right frontal temporal region and describes it as “dull” in nature. He has experienced occasional nausea but no vomiting with the headaches. Additionally, he has had difficulty focusing and concentrating on tasks at hand, such as reading the newspaper or playing cards. His wife states that he has been more irritable, moody, and “not himself” for 1 month. There is no history of alcohol abuse or exposure to toxins. He admits to a 30-pack-a-year smoking history. The review of systems is significant for weight loss and productive cough. His examination reveals that he is afebrile with a blood pressure of 124/72 mmHg and a heart rate of 78 beats/min. His general examination is normal. He is oriented to person, time, location, and situation, although he becomes upset during the examination. Cranial nerve and sensory examination findings are unremarkable. Motor strength testing is normal except for questionable weakness in the left finger extensors. The deep tendon reflexes are normal except for a Babinski sign present on the left. With ambulation, he has less arm swing on the left than the right. ◆ What is the most likely diagnosis? ◆ What is the next diagnostic step? ◆ What is the next step in therapy? Case analysis: In this case history there are some points that direct our attention that is is not a simple case of primary headache and there is underlying structural problem (red flags) Red flags in a case of headache 112 | P a g e 1) Subacute and progressive cause of headache 2) Severe headache “Thunderclap”. 3) New onset in adult life (>40years). 4) Change in headache pattern (increase in pain, increase in frequency, associated new features and low response to treatment) 5) Associated with unexplained nausea and vomiting. 6) Nocturnal headache and Awakening headache 7) Precipitation or worsening with Valsalva. 8) Confusion. 9) Seizures. 10) Abnormal neurological examination. 11) Presence of fever or signs of meningeal irritation. 12) Association with diminution of vision in one or both eyes. Now, try to check the different red flags in the previous case! Case 6-1 A 24-year-old white female has a 12-year history of headaches. These headaches started in grade school, and the patient remembers missing school with her headaches. Typically, she gets one of these headaches one to two times per month. The headache starts over the right eye, and the headache is usually preceded by flashing lights and zigzag lines. Once the headache occurs, there is extreme nausea and vomiting, and the patient goes into a dark room to minimize her head pain. Generally, the headache lasts 4 to 6 hours, but the patient feels tired and listless for the next 24 hours. The patient feels that the headache worsens with her menstrual cycle, and certain foods especially chocolates can exacerbate her headache. Her general and neurologic examinations are normal. ▪ What is the most likely diagnosis? ▪ What is the next diagnostic step? ▪ What is the next step in therapy? 113 | P a g e Case analysis: Clinical approach to a case of headache should include meticulous history taking to differentiate the different primary headache types that differ in nature of pain and associated symptoms. Secondary headache types should also be considered either metabolic or structural. Investigations help in determining the primary cause. There are some significant signs that must be considered as red flags when you deal with a case of headache which (if present) may raise the possibility of an underlying structural problem. When evaluating a patient for headache, the clinical history is of critical importance. The nature (type of pain and associated symptoms or triggers), severity, and duration of the headache is important in determining what type of headache it is and how to manage it. In this case, the patient has a prior history of headaches characterized as episodic and associated with nausea and vomiting, sensitivity to light (photophobia) and sound (phonophobia). Her examinations have been normal, and therefore, her clinical history is highly suggestive of a vascular or migraine headache. MIGRAINE Definition A paroxysmal primary headache disorder, characterized by recurrent intense throbbing headache that affects the head unilaterally or bilaterally usually associated with nausea, vomiting, photophobia or phonophobia. It may be preceded by visual, sensory and/or motor manifestations. Epidemiology: ▪ Migraine affects 1 in 10 people worldwide. ▪ More seen in females. F:M 3:1 114 | P a g e ▪ Migraines commonly begin between the ages of 15 and 25 and have an increased incidence in adults aged 35 to 45. Pathophysiology The mechanisms of migraine remain incompletely understood. The most accepted theory of migraine is the Neurovascular theory. Clinical picture Clinical types of migraine a) Migraine without aura [Common migraine]; most common type of migraine b) Migraine with aura [Classic migraine] Phases of migraine’s attack 1- Prodromal phase 2- Aura 3- Pain phase 4- Postdrome phase The prodrome phase Hours or days before the headache (altered mood, irritability, depression or euphoria, fatigue, yawning, excessive sleepiness, craving for certain food (e.g., chocolate), stiff muscles especially in the neck), increase urination, diarrhea and constipation). The aura Immediately precedes the headache. Aura comprises focal neurological phenomena that precede or accompany the attack. They appear gradually over 5 to 20 minutes. last less than 60 minutes 115 | P a g e TYPES OF AURA: ✓ Visual (Flashing of lights, scotomas, Zig-zag lines or Difficulty in focusing). ✓ Somatosensory The pain phase: The headache is initially unilateral and localized in the frontotemporal and ocular area, but pain can be felt anywhere around the head or neck. Pain intensity is moderate to severe. Throbbing in character. Intensifies with movement or physical activity. Many patients prefer to lie quietly in a dark room. The headache typically lasts from 4-72 hours. Associated symptoms. 1- Nausea and/or vomiting [1/3 of patients] 2- Photophobia and/or phonophobia The postdrome phase: The effects of migraine may persist for some days after the main headache has ended. Impaired thinking for a few days after the headache has passed. Tired or "hungover“. Head pain. Cognitive difficulties. Gastrointestinal symptoms. Mood changes. Weakness. Treatment A- Abortive therapy (During the attack) 116 | P a g e Pain relievers are most effective when administered early in the attack i.e., before the pain phase (a golden rule) ▪ Resting or sleeping in a dark room may help ease the symptoms faster. ▪ Over the counter migraine treatments: aspirin and paracetamol are often used. ▪ Non-steroidal anti-inflammatory drugs (NSAIDs) such as ibuprofen. ▪ Anti-sickness treatments: used along with pain killers at the onset of symptoms and in the case of troublesome nausea e.g., metoclopramide. ⧫ Triptans (first choice): It relieves pain by constricting blood vessels. It is a reasonable first choice for patients with moderate to severe disability from migraine. It can be given orally or subcutaneously. Mechanism of action: 5HT receptor agonist Examples: Sumatriptans Precautions of use: ischemic heart or cerebrovascular diseases. Not to be given with ergots. ⧫ Ergots: (less commonly used) Dihydroergotamine, an ergot derivative, is considered to be more effective with fewer side effects than ergotamine. B- Preventive Migraine Treatments These are groups of drugs that can be given to a patient to decrease the frequency of migraine’s attacks. Types of preventive therapy: Medical treatment o Antihypertensives: Beta blockers “propranolol” - Calcium channel blocker “verapamil” o Antidepressants: tricyclics “Amitriptyline” o Anti-epileptics: sodium valproate and Topiramate (drug of choice) 117 | P a g e  o Cyproheptadine: This drug may be used in children. o Monoclonal antibodies. Lifestyle modifications: o Maintain regular sleep patterns. o Eat regular meals. o Reduce/Limit Stress o Avoid “known” triggers (i.e., certain foods). TENSION-TYPE HEADACHE Epidemiology o Tension-type headaches (TTH) is the most common type of primary headache, with a prevalence in the general population about 40%. o More common in female [M:F 2:3]. Etiology Contraction of neck and scalp muscles 2ry to: ✓ Stress and/or anxiety ✓ Poor posture ✓ Depression Clinical Picture: Pain is: o Pressing or tightening (non-pulsatile quality) o Bilateral and occipitonuchal or bifrontal pain o Duration of 30 minutes to 7 days o No nausea or vomiting. o No Photophobia and/or phonophobia o Pain described as "fullness, tightness/squeezing, pressure," or "bandlike" o May occur acutely under emotional distress or intense worry 118 | P a g e  o Insomnia and difficulty concentrating o Often present upon rising or shortly thereafter o Muscular tightness or stiffness in neck, occipital, and frontal regions Treatment Lifestyle modification o Regular exercise, balanced meals, and adequate sleep. o Manage stress. o Avoid caffeinated drinks. Medications A triad of analgesics, antidepressants and muscle relaxants. CLUSTER HEADACHE Epidemiology o The least common of the 3 types of primary headache. o CH usually begins in middle adult life (30s – 40s). o CH is more common in males than in females; M:F=4:1. Clinical picture ⧫ Attacks of cluster headache (CH) are typically short and occur with a clear periodicity, Typically, a patient experiences 1-2 cluster periods per year, each lasting 2 weeks to 3 months. ⧫ The pain of CH is manifested as follows: o Character: Excruciating, stabbing, sharp, and lancinating (as if the eye is being pushed out), rather than throbbing o Location: Unilateral, in the periorbital, retro-orbital. The pain tends to remain on the same side during the cluster period. o Onset: Sudden, peaking in 10-15 minutes o Pain is accompanied by various cranial parasympathetic symptoms, including the following: 119 | P a g e  ✓ Ipsilateral lacrimation or conjunctival injection ✓ Nasal stuffiness or rhinorrhea ✓ Ipsilateral eyelid edema ✓ Ipsilateral miosis or ptosis ✓ Ipsilateral forehead and facial perspiration Treatment ABORTIVE TREATMENT o Inhalation oxygen via facial mask at 6 L/min o Corticosteroids: They are intended for intermittent use during acute flareups. PREVENTIVE TREATMENT o Lithium, Verapamil, Topiramate, Corticosteroids. Case 6-3 (test yourself) A 40-year-old male. The patient reports to physical therapy for a work-hardening evaluation that a company has requested in order to clear him for heavy labor. Halfway through the lifting evaluation, the patient immediately stops in the middle of the timed trial and sits down against the wall. When the therapist attends to the patient, he reports that he has been experiencing these “headache attacks” for the past month around this time of day. The patient is moved to a private treatment room with the lights off so that he may lie down and rest; however, he instead paces back and forth around the room. Once the patient is stable, the therapist begins to interview the patient on the nature of these headaches. The patient reports that since he started working late night shifts at the construction company one month ago, he was forced to nap throughout the afternoon in order to be safe to work in the early hours of the morning. However, when he would wake up, he would experience excruciating, burning pain above and behind his left eye. The pain was so severe that he could “feel something pulsating on the side of my head.” Once the pain subsided 20-30 minutes later, the patient looked in the mirror and saw that his left eyelid was red, swollen, and teary. The patient 120 | P a g e explains that these headaches have continued, and always seem to start after he wakes up at 5 p.m. (the time of this evaluation), approximately 3-4 times per week. When asked if lying down reduced the symptoms, the patient explained that laying down actually made the pain worse, so he is forced to pace around. However, when asked if his pain ever increases during an attack, the patient reports that the pain is often constant. In addition, the patient denies an increase in symptoms while staring at lights. The therapist asks if he ever feel nauseous, dizzy or confused. The patient denies any of these symptoms and believes these headaches are just “his body’s way of adjusting to the change in sleep patterns.” What is the most likely diagnosis? What is the next diagnostic step? What is the next step in therapy? 121 | P a g e  Clinical approach to “multiple sclerosis” Demyelinating Diseases: normal and healthy myelin is destroyed by a toxic, chemical or autoimmune substance e.g., multiple sclerosis.