Basic Neuroscience Cardinal Manifestation of Neurologic Disorders PDF

Basic Neuroscience Semester Cardinal Manifestation of Neurologic Disorders Dr. Linao |May 2020 OBJECTIVES...

Basic Neuroscience Semester Cardinal Manifestation of Neurologic Disorders Dr. Linao |May 2020 OBJECTIVES Anatomic Involvement: 1. Understand the clinical, physiologic and anatomic Clinical Manifestations (ex. Signs and symptoms) may be correlates of the neurologic signs and symptoms grouped as ff: 2. Develop skills in performing the neurologic history and 1. Disorders involving the cerebrum examination a. Abnormal mental status 3. Learn how to localize the neurologic symptoms or disease b. Cognitive and Language impairment process based on the clinical course or history and physical (re: higher cortical function) and neurologic findings c. Behavioral and emotional disorder d. Impairment of motor function Steps in the diagnosis of Neurologic Disorders e. Sensory impairment 1. Anatomic Diagnosis f. Visual Cortical impairment 2. Clinical Diagnosis or syndromic Diagnosis g. Seizures 3. Pathologic Diagnosis 4. Etiologic Diagnosis Impairment of higher cortical functions: 5. Functional Diagnosis The nature of impairment, i.e. memory loss, aphasia, acalculia, will be highly suggestive of lobe/s of the PE and NE cerebrum that was/were affected Always do complete examination! Level of sensorium (arousal) would indicate lesion The NE should confirm or verify the history location along the course of the ARAS, and the associated based on the clinical history: neurological symptoms will indicate at which level o Ex. Dx based on clinical history: Right frontal along its course was the ARAS affected lobe pathology with signs of increase ICP probably tumor. Disorders of Motility 1. Motor Paralysis Examples of Diagnosis: a. Pattern: 1. Lower motor neuron paralysis involving the left, acute i. Hemiplegia flaccid paralysis (AFP), due to an infection process, ii. Quadriplegia (Diplegia) probably Poliomyelitis vs other enteroviral infection, iii. Paraplegia with residual paralysis. iv. Monoplegia 2. Coma, secondary to brain Herniation due to right b. Associated Deficits: frontal tumor, probably metastatic tumor (Breast i. Facial Paralysis tumor as primary), Glasgow Coma Score (GCS) 6 ii. Other cranial nerve involvement iii. Sensory deficit The Purpose: Guide us in the appropriate diagnostic test to iv. Autonomic disturbance prescribe and in the prognostication for medium- and long-term c. Reflex management i. Normal ii. Exaggerated Cardinal Manifestation of Neurologic Disorders iii. Absent The clinical signs and symptoms suggestive of iv. Presence of abnormal reflexes neurological disorders can be grouped accd to the (Babinski Reflex) functions of the different parts of the nervous sys. d. Muscle Tone The clinical symptoms and signs are suggestive of a i. Normal disorder of function of specific part/s of the nervous ii. Flaccid sys. iii. Spastic/ Rigid e. Muscle Bulk Key points: i. Normal The clinical manifestations of the Pt with neurological ii. Atrophy disorders and Dx are based on the ff: iii. Hypertrophy o Area of the nervous system involved o Extent of the involvement of the Nervous sys o Nature and etiology of the neurologic disorder MD2023 1 of 7  Basic Neuroscience Cardinal Manifestation of Neurologic Disorders Upper vs Lower Motor Neuron Paralysis Negative Symptoms: Parkinson’s Disease Upper motor Neuron or Lower motor Neuron or Supranuclear Paralysis Infranuclear Paralysis Muscle affected in groups, Individual muscles may be never individual affected Atrophy slight and the Prominent muscle atrophy result of the Dx Spasticity with increased Flaccid paralysis with DTRs hypotonia and absent or decreased DTRs Presence of long tract No Babinski signs signs (Babinski sign) Parkinsonism comprises four cardinal motor features: Fasciculations absent Fasciculations may be 1. Bradykinesia- slow and small movements. Reduced present blink, face expression and gesturing. Soft voice. Normal NCV, no Abnormal NCV and EMG Difficulty getting out of chair, shuffling steps, and denervation potentials in findings (fibrillations/ reduced arm swing, freezing EMG fasciculations 2. Tremor- usually resting; “pill rolling”, often involves Psychogenic (Hysterical Paralysis) thumb 3. Rigidity- different from spasticity Patterns of weakness 4. Postural changes- Imbalance, fall; stooped flexed posture Tremor Branch Diagram Abnormality of Movement and Posture The Extrapyramidal Motor System (motor system of Types of Tremor the basal ganglia) o Modulation of movements is thru the interaction of the basal ganglia and cerebellar inputs to the pyramidal tract system (corticospinal and cortico-brainstem-spinal system). o Dysfunction would result to: ▪ Excessive involuntary Movements (Positive Symptoms) ▪ Slow Movements (Negative Symptoms) Motor Function of the Basal Ganglia Motor initiation and planning movements Adjusting speed and magnitude of movement Automatically implement of learned motor programs (walking, cycling etc.) Implementation of consecutive or simultaneous movements Adjustment of muscle tone Truncal Stability MD2023 2 of 7  Basic Neuroscience Cardinal Manifestation of Neurologic Disorders Movement Disorders 3. Athetosis Chorea, athetosis, ballism and dystonia: Is a slow continuous stream of slow, sinuous, writhing non-rhythmic involuntary movements may be movements, typically of the hands and feet. combinations of fragments of purposeful movements Most commonly seen together with chorea in dyskinetic and abnormal postures motor fluctuations in PD. All due to imbalance of activity in the complex basal Also in athetoid cerebral palsy where damage occurs in the ganglia circuits. basal ganglia. Sometimes also known as “Extrapyramidal disorders” Related to excessive dopaminergic activity. In PD reducing Primarily conditions related to excessive dopaminergic dopaminergic drugs alleviates activity in basal ganglia If athetosis becomes faster, it sometime blends with chorea, ie choreoathetosis/ choreo-athetoid movements. 1. Chorea (Latin choreus, dance) Can be thought of as an athetoid movement that gets stuck Jerky semi-purposive uncontrollable movements of limbs, for a period of time; thus, a patient with choreoathetosis face and trunks, increase with anxiety and disappear during may perform and involuntary movement in which his hand sleep and fingers are twisted behind his head. He may hold this In the limbs they resemble fidgety movements, and in the position for few moments before his hand move back n face, grimace front of his body. The parts of the movement when the limb Patients often attempt to conceal involuntary movements was held, unmoving, in an abnormal position would be by superimposing voluntary movements onto them e.g a considered a dystonia (may occur alone). involuntary movement of arm towards the face may adapted to look-like an attempt to watch 4. Ballismus Pathophysiology- structural lesions putamen, Globus Usually in elderly and ceases within few weeks usually self- pallidus and subthalamic nuclei-balance is critical between limited lasting 6-8 wks the direct and indirect motor pathways to produce normal More than dramatic ballistic movements of the arms and movement patterns legs on one side of the body (Unilateral) and therefore use term Hemiballismus. 2. Dystonia: Clinical features Treatment with antipsychotic is often effective Dystonia are sustained abnormal posture limbs, neck, Usually due to a CVA in contralateral subthalamic nucleus. trunk, tongue protrusion of fixed upward deviation of the eyes (oculogyric crisis). Due to co-contraction of agonist Incoordination and disorder of cerebellar function and antagonist muscles in part of the body. Classification: Function of the cerebellum: o Most common dystonia is focal (single body part); o Motor correction: adjusting movement on the fly affect one part of the body such as eyes, neck, arm or based on sensory and proprioceptive input. vocal cord. -- Usually idiopathic o Motor learning: improving performance motor o Multifocal dystonia: affects many different parts of the sequence with repetition body o Balance, coordinating muscle system across the body o Segmental dystonia- affect two adjoining parts of the body usually symptomatic Functional Organization of Cerebellar Outputs o Hemidystonia affects an arm and leg on one side of the body o Generalized dystonia affects most of the body, frequent involving the legs and back MD2023 3 of 7  Basic Neuroscience Cardinal Manifestation of Neurologic Disorders Functional organization of the cerebellar hemispheres o Cerebrocerebellum: motor planning and coordination o Spinocerebellum: Control of ongoing body and limb movements o Vestibulocerebellum: posture, balance, eye and movements Pain and other disorders of somatic sensation o In the evaluation of patients resenting with pain the following should guide the examiner: 1. Describe the character, intensity, duration, associated symptoms and location of the pain and radiation and distribution 2. Onset of symptoms: acute, subacute, chronic 3. Temporal profile: episodic or intermittent, persistent, acute and progressive, chronic and progressive vs chronic non progressive 4. Other associated signs and symptoms 5. Provoking and relieving factors Classification of pain and pain syndromes o Headache: Primary as in Migraine or Secondary due to tumor, CNS infection o Referred pain o Chronic pain o Pain secondary to other medical condition o Neuropathic pain o Central neurogenic pain o Pain associated with psychiatric conditions Nomenclature in the description of pain and abnormal sensation o Dysesthesia: Any abnormal sensation described as unpleasant by patient o Hyperalgesia: exaggerated pain response from a normally painful stimulus; usually includes aspect of summation wit h repeated stimulus of constant intensity and aftersensation MD2023 4 of 7  Basic Neuroscience Cardinal Manifestation of Neurologic Disorders o Hyperpathia: Abnormally painful and exaggerated reaction to a painful stimulus; related to hyperalgesia o Hyperesthesia (hypesthesia): Exaggerated perception of touch stimulus o Allodynia: abnormal perception of pain from a normally nonpainful mechanical or thermal stimulus: usually has elements of delay in perception and aftersensation o Hypoalgesia (hypalgesia): decreased sensitivity and raised threshold to painful stimuli o Anesthesia: reduced perception of all sensation, mainly touch o Pallanesthesia: loss of perception of vibration o Analgesia: loss of perception to pain stimulus o Paresthesia: spontaneous positive, prickling sensation that is not unpleasant; usually described as “pins and needles” o Causalgia: burning pain in the distribution of one or more peripheral nerves Sensory Disturbance MD2023 5 of 7  Basic Neuroscience Cardinal Manifestation of Neurologic Disorders Sensory Disturbances ▪ With Horner syndrome, anisocoria is more apparent in Positive Symptoms: dim illumination, and the affected pupil shows dilation lag. o Pain When the room light is abruptly turned off. o Hyperaesthesia: increase sensitivity to any stimulus ▪ Light and near pupillary reactions are intact, but the o Hyperalgesia: increased sensitivity to a painful eyelids is ptosis due to paresis of Muller muscle stimulus o Hyperpathia: increased sensitivity with increasing Abnormal Ocular movement: pain threshold to repetitive stimulation o Paraesthesia: “pins and needles sensation” , burning feeling o Dysaesthesia: inappropriate sensation to a stimulus o Allodynia: pain provokes by a non-painful stimulus Disorders of the ocular movement Dizziness and Vertigo Characteristics Peripheral Central Onset Sudden Gradual or sudden Intensity Severe Mild Duration Usually seconds or Usually weeks, minutes; months occasionally hours, (continuous) days (intermittent) but can be Abnormal pupillary size and reaction seconds or minutes with o Unreactive pupils vascular Causes o Small, poorly reactive pupils ( pinprick pupils”) Direction of One direction Vertical, ▪ Narcotic intoxication (can be iatrogenic) nystagmus (usually downbeating o “Blown Pupils” horizontorotatory) ▪ Rarely seen in ambulatory patient unless Effect of head Worsen by position, Little change, pharmacologically dilated – which may be position often single critical associated with surreptitiously be doing themselves position more than one ▪ When truly present, may indicate temporal position lobe herniation with third nerve compression – Associated None Usually present pt likely comatose. neurologic ▪ Findings o Horner Syndrome Associated May be present, none o A lesion any point along the oculosympathetic auditory findings including tinnitus pathway: o Which include: Coma and related disorders of consciousness ▪ Ptosis good history and neurologic examination to determine ▪ Miosis if the cause of coma is secondary to structural brain ▪ Enophthalmos lesion or metabolic ▪ Anhidrosis on the same side MD2023 6 of 7  Basic Neuroscience Cardinal Manifestation of Neurologic Disorders Seizure disorders and epilepsy Guide: Diagnosis of epilepsy and seizures is clinically based: history is the key to the correct diagnosis Cognition and Behavior symptoms Dementia Intellectual Disability Language Dysfunction Conduct and Behavior symptoms Summary Cardinal Manifestations of neurologic disorders may be classified or grouped accd to: ▪ Anatomical basis ▪ Functional basis MD2023 7 of 7  BASIC NEUROSCIENCE LECTURE : NEUROLOGIC EXAMINATION DATE: 03/02/2023 DR. PENASERADA 2ndSEMESTER A.Y. 2022-2023 NEUROLOGIC HISTORY  Chief complaint MINI-MENTAL STATUS EXAM  Onset  Focuses on a 10-min neurological  Circumstances surrounding the examination to determine the cognition of symptoms the patient  Duration  Best helpful in the monitoring for  Progression improvement or deterioration of dementia  Accompanying signs and symptoms  The total score is 30 NEUROLOGIC EXAMINATION MENTAL STATUS  Cornerstone in the evaluation of a  Mini mental status exam neurological patient  Orientation Must Haves:  Date  neurological hammer  Location  penlight  Registration  cotton  State three unrelated  tongue depressor items and ask patient to  stethoscope repeat  BP apparatus  Ask the patient to  ophthalmoscope remember the items since  pocket snellen chart it will be asked again later  tuning fork (128 or 256 Hz)  Attention and calculation  Begin with 100 and count LEVELS OF CONSCIOUSNESS backwards by subtracting 7’s LEVEL RESPONSE  If patient is unable to count, have them spell Alert Responds fully and the word WORLD appropriately to stimuli backwards Lethargic Drowsy, sluggish,  Recall opens eyes to verbal  Ask the patient to recall stimuli, responds to the 3 unrelated items question then falls  Language asleep  Naming Obtunded Opens eyes to vigorous  Repetition tactile stimuli,  3 step command responds slowly,  Reading confused, decreased  Writing interest in the  Copying environment  Mini-Mental Status Examination Stuporous Arouses from sleep o Dementia is classified as mild, only after painful moderate and severe stimuli o 26 to 30 – normal cognitive Comatose Unarousable with eyes function closed, unconscious o Between 20 to 25 – mild cognitive and unresponsive impairment 1 | DAAKS!  BASIC NEUROSCIENCE LECTURE : NEUROLOGIC EXAMINATION DATE: 03/02/2023 DR. PENASERADA 2ndSEMESTER A.Y. 2022-2023 o Between 10 to 19 – moderate o 0-9 – severe cognitive impairment  Fundoscopy CRANIAL NERVE EXAMINATION  Cup to disc ratio (1:2) CRANIAL NERVE III  Pupillary Responses  Pupil size and shape at rest CRANIAL NERVE I  Direct response  Test odor of coffee in each to light; consensual nostril response  Impairment can be due to nasal obstruction, damage to olfactory nerves, intracranial CRANIAL NERVE III, IV, VI lesions affecting olfactory bulb  Check eye movements in all directions CRANIAL NERVE II  Check smooth pursuit in horizontal and vertical directions  Visual acuity – each eye,  Test convergence use eye chart by moving object slowly toward nose CRANIAL NERVE V: TRIGEMINAL NERVE  Visual fields – fixate and Sensory Component report when a finger can be seen  ask the patient to moving into each quadrant; how close his/her eyes, a many fingers are shown in each tissue or pin is quadrant touched alternately to each side of the forehead, cheeks and chin and the patient is asked to compare sensations 2 | DAAKS!  BASIC NEUROSCIENCE LECTURE : NEUROLOGIC EXAMINATION DATE: 03/02/2023 DR. PENASERADA 2ndSEMESTER A.Y. 2022-2023 CRANIAL NERVE V Tuning fork used  Tested by touching each to differentiate neural cornea gently with a cotton wisp from mechanical  Observe any asymmetries hearing loss in the blink response CRANIAL NERVES IX, X MOTOR COMPONENT OF CN V GLOSSOPHARYNGEAL AND VAGUS NERVES  Ask the patient to clench  Let the patient his jaw and palpate for the say "ahh" or "kah" masseter and temporalis  The palate and muscles uvula should rise symmetrically in the back of the oral cavity CRANIAL NERVE VII  Paralysis of the ninth nerve causes a pulling of the uvula to  Look for asymmetry in the unaffected side facial expressions and depth of nasolabial folds  Facial weakness may be difficult to detect in cases where it is bilateral  Ask patient to smile, puff out cheeks, clench eyes tight, wrinkle their brow  Check taste with sugar solution on cotton swabs applied to each side of tongue CRANIAL NERVE IX, X CRANIAL NERVE VIII  Does the palate elevate symmetrically when say “Aah?”  Gag reflex  Simple hearing test, rub  Tests integrity of fingers near each ear CN 9 & 10, nuclei and muscles of pharynx 3 | DAAKS!  BASIC NEUROSCIENCE LECTURE : NEUROLOGIC EXAMINATION DATE: 03/02/2023 DR. PENASERADA 2ndSEMESTER A.Y. 2022-2023 CRANIAL NERVE XI  Scale 0/5 to 5/5 used  0/5 = no contraction  1/5 = muscle flicker but no movement  2/5 = movement possible; not against gravity  Shrug shoulders, turn  3/5 = movement possible against head in both directions and gravity but not against resistance raise head from bed against  4/5 = movement possible against force of your hand some resistance  5/5 = normal strength Deltoid (C5, C6) CRANIAL NERVE XII Axillary Nerve  Note any atrophy or fasciculations in the tongue muscles  Stick tongue straight out and note any deviation  Move tongue side to side and push against cheek Biceps (C5,  Unilateral lesion causes C6)Musculocutaneous deviation toward weak side nerve MOTOR EXAMINATION Triceps (C6, C7, C8) Radial Nerve Extensor Carpi Ulnaris (C7, C8) Posterior interosseous nerve 4 | DAAKS! BASIC NEUROSCIENCE LECTURE : NEUROLOGIC EXAMINATION DATE: 03/02/2023 DR. PENASERADA 2ndSEMESTER A.Y. 2022-2023 Dorsal Interosseous Quadriceps (C8, T1) (L2, L3, L4) Ulnar Nerve Femoral nerve Hamstrings Flexor Digitorum (C7, C8) (L5, S1, S2) Median Nerve Sciatic nerve Iliopsoas Tibialis anterior (L1, L2, L3) (L4, L5) Femoral Nerve Deep peroneal nerve Gastrocnemius, soleus Gluteus Maximus (S1, S2) (L5, S1, S2) Tibial nerve Inferior gluteal nerve Adductors (L2, L3, L4) Extensor hallucis longus Obturator nerve (L5, S1) Deep peroneal nerve Ask the patient to Gluteus medius and extend and raise both minimus, tensor fascia latae arms in front of them and (L4, L5, S1) keep their arms in place Superior gluteal nerve while they close their eyes and count to 10. Note for pronator drift 5 | DAAKS!  BASIC NEUROSCIENCE LECTURE : NEUROLOGIC EXAMINATION DATE: 03/02/2023 DR. PENASERADA 2ndSEMESTER A.Y. 2022-2023 SENSORY EXAMINATION VIBRATION  Place a vibrating tuning fork (usually 128 c/s) on a bony prominence  Ask the patient to indicate when the vibration, if felt, ceases  If impaired, move more proximally and repeat  Of value in the early detection of demyelinating disease and peripheral neuropathy PAIN/LIGHT TOUCH Instruct the patient to say “yes” when they feel the stimuli With the patient's eyes closed, alternately touch the patient with the needle or brush on each side of the body Instruct the patient to report if they notice 2-POINT DISCRIMINATION a difference in the strength of sensation on  Tested with a special type of caliper or 2 each side of their body pins/paper clips  Ask patient to close his eyes then touch him alternately with one or both points randomly  Ask patient if he feels one or two stimuli  Normal 2 point discrimination: 4-5 mm JOINT POSITION SENSE  Ask patient to close his eyes  Report if their large toe is "up" or "down" STEREOGNOSIS when the examiner manually moves the Ask the patient to close their eyes and patient's toe in the respective direction identify the object  Repeat on the opposite foot and compare you place in their hand Use common objects like a coin or pen Repeat this with the other hand 6 | DAAKS!  BASIC NEUROSCIENCE LECTURE : NEUROLOGIC EXAMINATION DATE: 03/02/2023 DR. PENASERADA 2ndSEMESTER A.Y. 2022-2023 GRAPHESTHESIA SENSORY EXAMINATION  Ask the patient to close their eyes and identify the number or letter you will write with the back of a pen on their palm  Repeat on the other hand with a different letter or number DEEP TENDON REFLEX EXTINCTION  Touch the patient in two places on opposite sides of the body, simultaneously  Ask the patient to point to where they felt sensation  Extinction is present if they only report feeling the sensation on one side of the body  4+ very brisk, hyperreflexive, with clonus  3+ brisker or more reflexive than normal  2+ normal  1+ hyporeflexive  0 areflexive ROMBERG’S TEST BABINSKI REFLEX  Stroke the lateral aspect across the ball of the foot  Ask the patient to remain  Note for the extension still and close her eyes of the big toe  (+) Romberg test  Positive Babinski o if a patient loses balance indicates an upper after standing still with their eyes motor neuron lesion closed 7 | DAAKS!  BASIC NEUROSCIENCE LECTURE : NEUROLOGIC EXAMINATION DATE: 03/02/2023 DR. PENASERADA 2ndSEMESTER A.Y. 2022-2023 CHADDOCK CEREBELLAR  used for testing cerebellar function (the cerebellum coordinates muscle actions to Stroke the lateral aspect produce organized activities such as of the foot (from external malleolus walking) to the small toe) with a blunt point Watch for dorsiflexion of the big toe  Ask patient to perform rapid alternating GORDON movements Firmly squeeze the calf Watch for dorsiflexion of great toe FINGER-TO-NOSE TEST OPPENHEIM Firmly press down on the shin and Patient is asked to run the thumb and the knuckles touch his/her own nose along the anterior medial tibia with their index toward the foot finger and then to touch Watch for dorsiflexion of the the examiner's finger great toe This movement is repeated several times COORDINATION AND GAIT HEEL-TO-SHIN TEST  Ask patient to repeatedly run the heel down the shin to the big toe  Look for jerky or wobbling movements or note if the heel constantly falls off to the side 8 | DAAKS!  BASIC NEUROSCIENCE LECTURE : NEUROLOGIC EXAMINATION DATE: 03/02/2023 DR. PENASERADA 2ndSEMESTER A.Y. 2022-2023 GAIT KERNIG’S SIGN  Allow patient to lie flat on the table, with  Natural the knee flexed.  On toes  Raise the upper leg until it is perpendicular  On heels to the floor and extend the lower leg while  Tandem along straight line keeping the upper leg stationary.  Let the patient walk across the  Positive when the patient raises their head room under observation or scream in pain while the maneuver is  Note length of step, width of base, done abnormal leg movements, instability (gait ataxia) and associated postural movements  Ask the patient to walk heel to toe (tandem walking) across the room to exaggerate any instability  Ask your patient to walk on their toes, then, on their heels  These can demonstrate weakness of the gastrocnemius and soleus and/or tibialis anterior MENINGES Neck Rigidity  Ask patient to touch chin to chest  Positive when patient feels pain upon doing so Brudzinski Test Neck is flexed Positive when the patient lifts leg off the table or flexes the neck due to pain 9 | DAAKS!  MD 2 ☤ LECTURE 4: CVD (CEREBROVASCULAR DISEASE) & STROKE Dr. Linao| SEM 1 | 09-11-24 OBJECTIVES 1. Understand the pathophysiologic mechanisms in Stroke  Cerebrum (Yellow) 2. Types of Stroke 1. Middle Cerebral Artery 3. Causes  Continuation of Internal Carotid 4. Evaluation Artery 5. Diagnostic and Therapeutic management 2. Anterior Cerebral Artery  Connected by Anterior EPIDEMIOLOGY (AHA) communicating artery 3. Posterior Cerebral Artery Stroke  Posterior communicating artery connects PCA to MCA  Someone in the US has a stroke every 40 seconds on average. In 2016, stroke accounted for about 1 of every 19 deaths in the US.  On average in 2016, someone died of stroke every 3 minutes 42 seconds.  When considered separately from other cardiovascular diseases, stroke ranks No. 5 among all causes of death in the US, killing approximately 142,000 people a year. CIRCLE OF WILLIS: CEREBRUM 1  CIRCLE OF WILLIS: CEREBELLUM AND  Unique -> does not follow the arterial supply BRAINSTEM  Cerebrum, Cerebellum and Brainstem empty into Dural Venous Sinuses  Spinal Cord drain into Internal and External Vertebral Plexuses DURAL VENOUS SINUS  Between the periosteal and meningeal layers of the dura mater  Drains into the internal jugular vein  “Collecting pools” of blood from the 1. CNS (cerebrum, cerebellum and brainstem) 2. Scalp 3. Face  “Valveless” DEFINITION OF TERMS:  Stroke  sudden focal neurologic syndrome, specifically caused by cerebrovascular disease  Cerebrovascular disease brain abnormality resulting from a pathologic process involving the cerebral vasculature: 1. occlusion of the lumen 2. rupture of the blood vessel wall 3. an altered permeability of the blood vessel wall 4. changes in the viscosity or the quality of the blood flowing thru the cerebral blood vessels MECHANISM OF ISCHEMIC STROKE AND Cerebellum (Purple) TRANSIENT ISCHEMIC ATTACKS 1. Superior Cerebellar – from Basilar 2. Anterior Inferior Cerebellar Artery (AICA) – from Basilar 3. Posterior Inferior Cerebellar Artery (PICA) – from Vertebral  Atherosclerotic cerebrovascular disease (20%): 1. Extracranial carotid or vertebral artery disease Brain stem (Pink) Pontine Branches – from Basilar 2. Intracranial cerebrovascular disease Anterior Spinal Artery – from Vertebral  Penetrating small arterial disease (25%)  Cardiogenic source (33%): VENOUS DRAINAGE OF CNS 1. Atrial fibrillation & other arrythmias 2. Myocardial infarction 3. Valvular disease 4. Ventricular thrombi 5. Aortic plaque  Unusual causes (arm weakness, grasp  Cognitive: muteness, perseveration, abulia, disinhibition ETIOLOGY OF ISCHEMIC STROKE:  PCA:  Hemianopia LARGE VESSEL EMBOLIC:  Cognitive: memory loss/confusion, alexia  The Heart  Cerebellum: o Valve diseases, A. Fib, Dilated  Ipsilateral ataxia cardiomyopathy, Myxoma Abulia - Loss or impairment of the ability to make decisions or  Arterial Circulation (artery to artery emboli) act independently o Atherosclerosis of carotid, Arterial dissection, Anosonosia - complete unawareness or denial of a neurologic Vasculitis deficit.  The Venous Circulation o PFO w/R to L shunt, Emboli 3  CORTICAL SIGNS  Face Drooping  Does one side of the face droop or is it numb? Ask the person to smile. RIGHT BRAIN: LEFT BRAIN:  Arm Weakness  Is one arm weak or numb? Ask Right gaze preference Left gaze preference the person to raise both arms. Does one arm drift Neglect Aphasia downward?  If present, think LARGE VESSEL stroke  Speech Difficulty Is speech slurred, are they BRAINSTEM STROKE SYNDROMES unable to speak, or are they hard to understand? Ask the person to repeat a simple sentence, like "the sky  Rarely presents with an isolated symptom is blue." Is the sentence repeated correctly?  Usually a combination of cranial nerve abnormalities,  Time to call 911  If the person shows any of these and crossed motor/sensory findings such as: symptoms, even if the symptoms go away, call 9-1-1 and get them to the hospital immediately.  Double vision  Facial numbness and/or weakness ACUTE ONSET OF ANY OF THE BELOW  Slurred speech SYMPTOMS  Difficulty swallowing  Ataxia  Hemiparesis or quadriparesis (  Vertigo latter in basilar occlusion)  Nausea and vomiting  Facial weakness  Hoarseness  Aphasia TRANSIENT ISCHEMIC ATTACK (TIA)  Dysarthria  Limb/truncal/gait ataxia +/- nausea  Definition: duration of transient neurologic symptoms & vomiting lasting less than 1 hour  Vertigo, tinnitus, hearing deficit (posterior circ.)  Transient reduction of blood flow to a region in brain in the  Impairment of vision in homonymous visual field absence of evidence of infarction on brain imaging defect  Monocular impairment of vision (amaurosis fugax)  Mechanisms for TIA similar as for ischemic stroke  Diplopia  Reconstitution of flow to the hypoperfused region hence  Impairment or loss of consciousness or confusion the resolution of symptoms  Hemineglect (visual or sensory)  Significance of TIAs is increased risk of stroke after a TIA  Headache (non-specific symptom) specifically early on after a TIA  New onset seizure (3-4%) or acute new movement abnormality  Prompt evaluation of mechanism and appropriate treatment NIHSS- (NATIONAL INSTITUTE OF HEALTH STROKE SCALE ) SIGNS AND SYMPTOMS OF STROKE:  Standardized method used by health care professionals to ACUTE ONSET OF NEUROLOGIC SYMPTOMS AND measure the level of impairment caused by a stroke SIGNS OF CENTRAL NERVOUS SYSTEM  Purpose INVOLVEMENT o Main use is as a clinical assessment tool to determine whether the degree of disability is severe enough to ] warrant the use of tPA (tissue Plasminogen Activator) o Another important use of the NIHSS is in research, where it allows for the objective comparison of efficacy across different stroke treatments and rehabilitation interventions  Scores are totaled to determine level of severity of stroke  Can also serve as a tool to determine if a change in exam has occurred 4  NIHSS INTERPRETATION CASE 1  74 year old female with sudden onset of left-sided weakness  She was at church when she noted left facial droop  History of HPN and atrial fibrillation  Meds: Losartan  BP- 172/89, P– 104, T- 98.0, RR– 22, O2- 94%  General exam: Unremarkable except irregular rate and rhythm  NEURO EXAM: NIHSS AND OUTCOME PREDICTION  Speech dysarthric but language intact  Right gaze preference  NIHSS below 12-14 will have an 80% good or excellent  Left facial droop outcome  Left- sided hemiplegia  Neglect  NIHSS above 20-26 will have less than a 20% good or excellent outcome  Lacunar infarct patients had the best outcomes DIFFERENTIAL DIAGNOSIS  Space occupying lesion (tumor, infection/ abscess, Epidural, Subdural Hematomas)  Subarachnoid hemorrhage  Seizures  Hypoglycemia  Migraine  Syncope  Labyrinthine disorders APHASIA  Broca’s  Right MCA infarct, most likely cardioembolic from atrial fibrillation o Expressive aphasia  Patient underwent mechanical thrombectomy with intra-arterial verapamil, clot removal successful o Left posterior inferior  Excellent recovery – patient was discharged 48 hours later on Coumadin o frontal gyrus  Wernicke’s CASE 2 o Receptive aphasia  85 year old male who woke up with left face, arm, and leg o Posterior part of the superior temporal gyrus numbness o Located on the dominant side  History of HTN, DM, and tobacco use 5  Meds: Insulin, aspirin CASE 4  BP- 168/96, P– 92  56 year old female who upon waking post-op after elective surgery was found to have L sided weakness  General exam: Unremarkable, RRR and neglect  NEURO EXAM:  History of HTN  Decreased sensation on left face, arm, and leg  Meds – Lisinopril  BP- 132/74, P– 84  General exam: Unremarkable, RRR  NEURO EXAM:  Left face, arm, and leg weakness  Neglect  DTR’s brisk on the left, toe up on left  Right thalamic lacunar infarct  Discharged to rehab 72 hours after admission CASE 3  55 year old male with acute onset of right sided numbness and tingling, left sided face pain and numbness, gait imbalance, nausea/vomiting, vertigo, swallowing difficulties, and hoarse speech  History of CAD s/p CABG, DM2, HTN, HLD, OSA  Meds: Aspirin,clopidogrel, insulin, lipitor, metoprolol, lisinopril  NEURO EXAM: BP- 194/102, P– 105  General exam: Unremarkable, RRR  NEURO EXAM:  Decreased sensation on left face  Decreased sensation on right body  Left ataxia on FNF, and unsteady gait  Voice hoarse  Nystagmus  Right hemisphere watershed infarct secondary to hypoperfusion in the setting of Right ICA stenosis  On review of anesthesia records, blood pressure  Brainstem Stroke dropped to 82/54 during the procedure  Received IV tPa  Patient was discharged to in-patient rehab  Post-tPa symptoms greatly improved regained sensation, ataxia resolved  Discharged home with out patient PT/OT 6  INTRACRANIAL HEMORRHAGES CEREBRAL HEMORRHAGE ETIOLOGY OF ICH  Traumatic  Spontaneous o Hypertensive o Amyloid angiopathy o Aneurysmal rupture o Arteriovenous malformation rupture o Bleeding into tumor o Cocaine and amphetamine use CAUSES OF ICH CEREBELLAR HEMORRHAGE  Vomiting (more common in ICH than SAH or Ischemic CVA) HYPERTENSIVE ICH  Ataxia  Eye deviation toward the opposite side of the bleed  Spontaneous rupture of a small artery deep in the  Small sluggish pupils brain o Typical sites  AMS o Basal Ganglia PONTINE HEMORRHAGE o Cerebellum o Pons  Pin-point but  Typical clinical presentation reactive pupils o Patient typically awake and often stressed,  Abrupt onset of then abrupt onset of symptoms with acute coma decompensation  Decerebrate posturing or GANGLIONIC BLEED flaccidity  Ataxic breathing  Contralateral hemiparesis pattern  Hemisensory loss  Homonymous hemianopia  Conjugate deviation of eyes toward the side of the bleed or downward 7  SUBARACHNOID HEMORRHAGE MANAGEMENT  “Worst headache of my life”  The primary objective is to restore adequate cerebral perfusion to ensure adequate cerebral metabolism  AMS and function: 1. Airway for adequate oxygenation  Photophobia 2. BP - maintain mean arterial pressure 3. Normal glucose level  Nuchal 4. Avoid hyperthermia rigidity BLOOD PRESSURE MANAGEMENT  Seizures  The goal is to maintain cerebral perfusion!!  Nausea  CPP = MAP – ICP (needs to be at least 70) and  Higher BP goals with Ischemic stroke MAP 110-130 mm vomiting Hg  Lower BP goals with Hemorrhagic stroke (avoid hemorrhagic expansion, especially in AVMs and aneurysms) < 160 mmHg systolic INITIAL EVALUATION For the most part, ICH stroke guidelines recommend using IV medications to lower SBP < 160 while still maintaining adequate  Cardiac monitoring, pulse-ox, ECG MAP and CPP  Stat CT brain Ischemic strokes are a bit trickier to manage. One must keep in mind that the patient’s blood pressure will lower on its own by  c-xray approximately 25 – 30 % within the first 24 hours. Furthermore aggressive treatment of hypertension in ischemic  CBC, Platelet, PT, PTT strokes has been shown to worsen neurological function by reducing perfusion pressure  blood glucose, serum electrolytes Castillo and collegues performed a study in 2004 that showed that a drop in either SBP or DBP > 20 points were associated with  Cardiac markers, ABG’s higher rates of mortality and larger volumes of infarctions. They also noted that early administration of antihypertensinve  Blood alcohol level, Toxicology screen, Pregnancy test( as medications to patients with SBP > 180 was associated with an necessary) increased risk of death. **** CHHIPS trial *** IMAGING According to the guidelines, sbp should be reduced by 15 – 25% within the first day as excessively high blood pressures are CT SCAN associated with an increased risk of hemorrhagic conversion.  Non- contrast CTH remains the gold standard as it is superior for showing IVH and ICH B P-AIS RELATIONSHIP  CT with contrast may help identify aneurysms, AVMs, or tumors but is not required to determine whether or not the  BP increase is due to arterial occlusion (i.e., an effort to perfuse penumbra) patient is a tPa candidate MRI  Failure to recanalize (w/ or w/o thrombolytic therapy) results in high BP and poor neuro  Superior for showing underlying structural lesions outcomes Penumbra  Contraindications Core  ANGIOGRAPHY  Lowering BP starves penumbra, worsens outcomes Interestingly, although the head CT is considered the standard for  In AIS, high BP is a patients with suspected strokes, it is used to not to confirm an acute response ischemic stroke but instead rule out other causes of the patient’s condition. CTs are relatively insensitive for detecting acute and small cortical infarctions especially in the posterior fossa region. Clot in Artery However, if there is evidence of early edema or mass effect noted on the initial head ct, the patient’s risk of hemorrhagic conversion increases by approximately 8 fold. 8  Scwartz and collegues published a study in 200 that stated patients who survived the first 72 hours after hospital admission, the duration of fever is realted to outcome and is a an independent prognostic factor in stroke patients. However, although there have been several studies done, to date there is no recommended drug or dose of medication that is recommended in the treatment of fevers in stroke patients. Guidelines currently recommend that clinicians seek out a souce (don’t just assume that the fever is neurogenic in nature) and treat accordingly. SUPPORTIVE THERAPY ACUTE THERAPY  Glucose Management  NINDS Stroke Study group: randomized placebo controlled clinical trial (N Engl J Med 1995) o Infarction size and edema increase with acute  Intravenous recombinant tissue Plasminogen and chronic hyperglycemia Activator (IV t-PA) given within 3 hour of symptoms o Hyperglycemia is an independent risk factor for onset in acute ischemic strokes hemorrhage when stroke is treated with t-PA  N=624 patients (IV t-PA or placebo):dose 0.9mg/kg, 10% IV bolus, then the remainder is IV drip over 1 hour  Antiepileptic Drugs o Seizures are common after hemorrhagic CVAs NINDS STROKE STUDY  Patients in the t-PA arm were at least 30% more likely to o ICH related seizures are generally non- have minimal or no disability at 3 months convulsive and are associated to with higher  Symptomatic Intracranial Hemorrhage was 6.4% in the t- NIHSS scores, a midline shift, and tend to predict PA group versus 0.6% in the placebo arm poorer outcomes  Mortality at 3 months was not statistically different Elevated glucose levels at the time of admission predicts between t-PA and placebo an increased 28 day mortality rate in both diabetic and non-  The benefit of IV t-PA was sustained at one year follow up diabetic patients.  The earlier the treatment the better the outcome Study done by Vespa and collegues done in 2003  IV T-PA TREATMENT showed that 18 / 63 patients ( 28% ) of patients in a neuro ICU seized on EEG within 72 hours of admission  IV t-PA was FDA approved for acute ischemic stroke Rx based on the NINDS study group ICH stroke guidelines recommend IV medications to  Inclusion and Exclusion criteria quickly stop seizures. Benzos tend to be first line choice, followed by IV phenytoin or fos-phenytoin, Brief period of INTRAVENOUS T -PA prophylactic AED therapy has been shown to redice the risk of early seizures esp in patient with lobar hemorrhage.  Standard FDA approved therapy for acute stroke Rx HYPERTHERMIA  Window of treatment has been prolonged after ECASSIII to 4.5 hours  Treat fever!  Not all patients are eligible for the 3 to 4.5 hour  Evidence shows that fever > 37.5 C that window persists for > 24 hrs correlates with INCLUSION CRITERIA FOR IV T-PA ventricular extension of the bleed and is  Ischemic Stroke clinically found in 83% of patients with poor outcomes  Persistent neurologic deficit beyond an isolated sensory deficit / ataxia Fevers tend to be more common in basal ganglia and lobar  CT brain: No Blood ICHs and patients with IVH.  Initiation of Rx within 3 hours 9 EXCLUSION CRITERIA NIH STROKE SCALE  Onset to treatment >3 hr (NINDS)  Designed for acute stroke trials.  Rapid improvement  Blood on CT  Quick (5-10 min) & reproducible.  Oral anticoagulant & PT>15 sec, INR>1.7  Requires speech/language cards & safety pin.  Heparin (last 48 hr) & increased PTT  Quantifies clinical stroke deficit:  Platelet110  Aggressive treatment of b.p.  > 15 = poor prognosis if no treatment  Stroke or head trauma (3 months)  > 22 =  risk for ICH  Major surgery (2 wks)  Prior ICH  GI tract/ Urinary bleed (14 d) STROKE IS PREVENTABLE, BEATABLE AND  Seizure at onset TREATABLE!  Signs & Sx’s of SAH  Non-compressible site of arterial puncture (7d)  80% of all strokes can be prevented with healthy behaviors ADDITIONAL EXCLUSIONS FOR THE 3 TO 4.5 HOUR  Long-term effects of a stroke may be minimized with immediate treatment  Age≥80 years  More people are surviving and beating stroke  Any use of anticoagulant regardless of the PT/PTT OTHERS STROKE SYMPTOMS  NIHSS≥25  Coexistent history of stroke and diabetes mellitus  Sudden numbness or weakness of the leg  Sudden confusion or trouble understanding MANAGEMENT POST THROMBOLYSIS  Sudden trouble seeing in one or both eyes  Sudden trouble walking, dizziness, loss of balance or  Admit to ICU coordination  BP monitoring (Q 15 m x2 h, Q 30 m x6 h, Q 1 h x16 h)  Sudden severe headache with no known cause  Treat SBP≥185 and DBP≥110  No anticoagulants, no anti-platelet for 1st 24 hr post t-PA  Worsening of neurologic state---CT brain  ICH---Neurosurgery consult  Possible surgical intervention PREVENTION  Preferably: no foley or NG for 2 hr > t-PA (t1/2-t-PA = 8- 12 min) PRIMARY PREVENTION NIH STROKE SCALE  Primary prevention starts at the level of the physician playing the role of the primary care and occasionally at “Traditional” order of items” the level of the cardiologist and the stroke neurologist  Key is identification of underlying risk factors and 1a. LOC 5b. Left arm motor modification and treatment of modifiable risk factors 1b. LOC questions 6a. Right leg motor PRIMARY PREVENTION ELEMENTS 1c. LOC commands 6b. Left leg motor  Establishing good medical history and family history 2. Best gaze 7. Limb ataxia 8. Sensory  Identifying the patient’s vascular risks including medical 3. Visual fields illnesses, habits such as smoking and substance use and 9. Best language genetic predisposition through review of significant family 4. Facial palsy 10. Dysarthria history for cardiovascular risk factors and stroke 11. Extinction/ inattention 5a. Right arm motor  Exam elements which are key: pulse (rate and establishing how regular), blood pressure, carotid auscultation (bruits), cardiac auscultation (murmurs and 10  abnormal rhythm), symmetry and detection of pulses,  Cardiac disease: Atrial Fibrillation, Myocardial infarction diabetic peripheral changes. secondary to coronary artery disease  Dyslipidemia or hyperlipidemia (high cholesterol, high IDENTIFICATION OF RISK FACTORS FOR STROKE LDL, low HDL)  Migraine with aura in women MODIFIABLE RISK FACTORS  Obstructive sleep apnea  Risk factors that can be controlled by life style changes or by medications or surgery LESS-DOCUMENTED POTENTIALLY MODIFIABLE NON -MODIFIABLE RISK FACTORS RISK FACTORS  Age: the risk of stroke doubles with every decade  Obesity after the age of 55 years  Lack of exercise  Sex: lifetime risk in Male>Female but risk in F>M  Poor diet after age of 80 years  Alcohol abuse  Race and ethnicity:  Hyperhomocystei-nemia  Illicit drug abuse o Stroke incidence and subtypes: higher in African Americans and Hispanics >Caucasians  Hypercoagul-opathy  Sickle cell disease o Stroke related mortality is higher in African American population  Estrogen/HR hormonal therapy  Inflammation o Asian population has an increased risk of hemorrhagic stroke subtype compared to  Infection Caucasians ---------------------  80% of all Strokes Are Preventable NON -MODIFIABLE RISK FACTORS GENETIC FACTORS REDUCE YOU STROKE RISK  Family history: inherited susceptibility, inherited  Control high blood pressure predisposition to risk factors, similar culture and lifestyle  Don’t smoke  Consume less sodium  Hyperhomocysteinemia: C677T allele (one or more) of  Lower cholesterol the methylenetetrahydrofolate reductase gene (MTHF)  Lose excess weight  Get physically active  Inherited coagulopathies: o FV Leiden mutations, prothrombin gene mutation o PC, PS deficiencies o Anticardiolipin antibodies/LA are genetic in 10% cases o Others  CADASIL: Cerebral autosomal dominant arterof iopathy with subcortical infarcts and leukoencephalopathy: NOTCH 3 gene mutation on chromosome 19  Others: Marfan and NF I and II, Fibromuscular dysplasia (FMD), Ehlers-Danlos syndrome IV, polycystic kidney disease  Novel genes identified which may have specific associations with large artery stroke WELL DOCUMENTED MODIFIABLE RISK FACTORS  Hypertension  Smoking  Diabetes Mellitus  Carotid disease 11