Diagnostic Approach to hemiplegia

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Clinical Approach to Hemiplegia:

Clinical Approach to Hemiplegia - Dr Manish Chandra Prabhakar MGIMS 1 Reference- Harrison's International Medicine

DDs Hemiparesis:

DDs Hemiparesis Stroke Focal seizures ( Todd’s Palsy) Migraine Intracranial neoplasm, Cerebral abscess Head injury Subdural hematoma Epidural hematoma Hyperglycemia , Hypoglycemia Acute conversion reaction Focal encephalitis,meningitis Drug overdose –cocaine, amphetamine Hypertensive encephalopathy Metabolic encephalopathy Cardiac syncope or syncope from other causes Postcardiac arrest ischemia 2 Reference- Harrison's International Medicine

PowerPoint Presentation:

Comments Diagnosis Focal deficits likely are caused by seizure-induced neuronal dysfunction (reversible). May occur with simple partial or generalized seizures. Spontaneous resolution occur over hours (may last up to 48 hours) Seizures (postictal) Aphasia or hemiplegia may be present. Variable drowsiness or obtundation. Blood glucose usually <45 mg/dl. Resolution of symptoms with IV glucose. Hypoglycemia Etiologies include hyperosmolar hyperglycemia, hyponatremia, and hepatic encephalopathy. May be associated with altered level of consciousness, poor attention, or disorientation (eg, delirium) asterixis. Metabolic encephalopathy Diagnosis of exclusion. Conversion disorder is the most common psychiatric diagnosis. Comorbid psychiatric problems are common. Paresis, paralysis, and movement disorders are common. Conversion reaction Imaging evidence or history of remote stroke is often apparent. Previous deficit may have resolved completely. Reactivation of prior deficits 3

Bedside Assessment:

Bedside Assessment History Neurologic examination 4 Reference- Harrison's International Medicine

History:

History The time of symptom onset If patient is able to provide information family or friends The nature of symptoms Abruptly: vascular etiology Risk factors for vascular disease, history of seizures , migraine, insulin use or drug abuse Accompanying symptoms (severe ‘thunderclap’ headache  subarachnoid Hemorrhage) 5 Reference- Harrison's International Medicine

Important Historical information in the Suspected Stroke Patient:

Important Historical information in the Suspected Stroke Patient History of the Present Illness Time of symptom onset Evolution of symptoms, recovery Convulsion or loss of consciousness at onset Headache Chest pain at onset Medical History Prior intracerebral hemorrhage, h/o stroke, Recent head trauma h/o myocardial infarction Surgical History- Recent surgical procedures Medications- Anticoagulant therapy Review of Systems- Gastrointestinal or genitourinary bleeding 6 Reference- Harrison's International Medicine

History (cont’d):

History (cont ’ d) Record: Vital signs Blood glucose level of consciousness severity of deficits Presence of bowel or bladder incontinence 7 Reference- Harrison's International Medicine

Neurologic Examination:

Neurologic Examination Identify signs of lateralized hemispheric or brainstem dysfunction consistent with focal cerebral ischemia. Level of consciousness, the presence of a gaze deviation, aphasia, neglect or hemiparesis 8 Reference- Harrison's International Medicine

NIH Stroke Scale (NIHSS):

NIH Stroke Scale (NIHSS) Validated 15-item scale used to assess key components of the standard neurologic examination and measure stroke severity ( lyden et al, 1999) It assess level of consciousness, ocular motility, facial and limb strength, sensory function, coordination , language, speech and attention. Scores range from 0 (normal) to 42 (maximal score). It predicts short-term and long-term neurologic outcomes . (Adams et al, 1999) 9 Reference- Harrison's International Medicine

NIH Stroke Scale:

NIH Stroke Scale 0= Alert 1= Not alert, arousable 2= Not alert, obtunded 3= Unresponsive 1a. Level of consciousness 0= Answers both correctly 1= Answer once correctly 2= Answer neither correctly 1b. Questions 0= Performs both tasks correctly 1= Performs one task correctly 2= Performs neither task 1c. Commands 0= Normal 1= Partial gaze palsy 2= Total gaze palsy 2. Gaze 0= No visual loss 1= Partial hemianopsia 2= Complete hemianopsia 3= Bilateral hemianopsia 3. Visual fields 0= Normal 1= Minor paralysis 2= Partial paralysis 3= Complete paralysis 4. Facial palsy 0= No drift 1= Drift before 10 seconds 2= Falls before 10 seconds 3= No effort against gravity 4= No movement 5a. Left motor arm 0= No drift 1= Drift before 10 seconds 2= Falls before 10 seconds 3= No effort against gravity 4= No movement 5b. Right motor leg 0= No drift 1= Drift before 5 seconds 2= Falls before 5 seconds 3= No effort against gravity 4= No movement 6a. Left motor leg 0= No drift 1= Drift before 5 seconds 2= Falls before 5 seconds 3= No effort against gravity 4= No movement 6b. Right motor leg 0= Absent 1= One limib 2= Two limbs 7. Ataxia Scale Definition Category Scale Definition Category 10 Reference- Harrison's International Medicine

NIH Stroke Scale:

NIH Stroke Scale 0= Normal 1= Mild loss 2= Severe loss 8. Sensory 0= Normal 1= Mild aphasia 2= Severe aphasia 3= Mute or global aphasia 9. Language 0= Normal 1= Mild 2= Severe 10. Dysarthria 0= Normal 1= Mild 2= Severe 11. Extinction/inattention Scale Definition Category 11 Reference- Harrison's International Medicine

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Cardio-vascular system Carotid bruit Cardiac murmur Irregularly irregular heart rhythm Unequal extremity pulses Other – Signs of head or neck trauma (occult cervical spine injury) Rales on chest examination (Pneumonia) Bilateral asterixis (metabolic encephalopathy). 12 Reference- Harrison's International Medicine

WHO definition: Stroke:

WHO definition: Stroke “a neurological deficit of sudden onset accompanied by focal dysfunction and symptoms lasting more than 24 hours that are presumed to be of a non-traumatic vascular origin” 13 Reference- Harrison's International Medicine

Definitions of Stroke:

Definitions of Stroke Transient Ischemic Attack Stroke in evolution RIND ( Reversible Ischemic Neurological Deficit) 14 Reference- Harrison's International Medicine

TIA:

TIA Brief episodes of focal neurological deficits lasting 2-3 minutes to at most a few hours but no longer than 24 hours leaving no residual deficits with complete functional recovery. 15 Reference- Harrison's International Medicine

Reversible Ischemic Neurological Deficit (RIND):

Reversible Ischemic Neurological Deficit (RIND) a focal brain ischemia in which the deficit improves over a maximum of 72 hours deficits may not completely resolve in all cases 16 Reference- Harrison's International Medicine

Stroke in evolution:

Stroke in evolution An unusual condition in which a restricted neurological deficit spreads relentlessly over a small period of time, usually hours, to involve adjacent functional areas supplied by the affected artery. 17 Reference- Harrison's International Medicine

Major risk factors:

Major risk factors Hypertension ( Systolic or diastolic) Smoking Atrial Fibrillation Myocardial Infarction Hyperlipidemia Diabetes Congestive Heart Failure Acute Alcohol abuse TIA >70% occlusion of the carotid arteries Oral contraceptives in women Hypercoagulopathy Polycythemia and Hemoglobinopathy Age, Gender(Male : Female 3:2), Race, Prior Stroke, and Heredity 18 Reference- Harrison's International Medicine

Stroke in the young Pt:

Stroke in the young Pt 3-4% of strokes occur in people aged 15-45 Sickle Cell anemia, tuberculosis Hypercoaguable states Pregnancy, OCP use, antiphospholipid antibodies, protein C and S deficiencies,nephrotic syndrome Drugs Cocaine, amphetamines 19 Reference- Harrison's International Medicine

Classification of Stroke:

Classification of Stroke Ischemic (85 % of stroke, Embolic or Thrombosis) Hemorrhagic (15% of stroke) 20 Reference- Harrison's International Medicine

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Acute Stroke Ischemic ( 85%) Hemorrhagic (15%) Intracerebral & Cerebellar H Subarachnoid H. Subdural & Extradural H. and Hematoma Thrombotic ( 55%) Embolic (30%) Cardioembolic Artery-artery embolism AF, IHD, VHD, Lacunar (20%) Large vessel ( 35%) 21 Reference- Harrison's International Medicine

Ischemic: Thrombotic local origin of clot:

Ischemic: Thrombotic local origin of clot Usually develops at night during sleep Symptoms perceived in morning Suspect in h/o hypercoaguable states , atherosclerosis and collagen vascular disorders 22 Reference- Harrison's International Medicine

Ischemic: Embolic proximal origin of clot:

Ischemic: Embolic proximal origin of clot Occurs at any time Frequently during periods of vigorous activity Hx of Atrial fibrillation, valvular vegetations, thromboembolism from MI, ulcerated plaques in carotid system Seizures in 20% of cases

Causes:

Causes 24 Reference- Harrison's International Medicine

Hemorrhagic Stroke:

Hemorrhagic Stroke 25 Reference- Harrison's International Medicine

Hemorrhagic Stroke:

Hemorrhagic Stroke Occur during stress or exertion Focal deficits rapidly evolve Signs of raised ICT Confusion, coma or immediate death 26 Reference- Harrison's International Medicine

Hemorrhagic or Ischemic:

Ischemic Hemorrhagic Loss of Consciousness -ve +ve Headache -ve +ve Vomiting -ve +ve Previous TIA +ve -ve Gradual Onset +ve -ve (Sudden and maximal) Relation with activity -ve +ve BP -ve/mild Moderate/ Severe Bloody CSF -ve +ve Hemorrhagic or Ischemic 27 Reference- Harrison's International Medicine

Localization of Stroke:

Localization of Stroke . 28 Reference- Harrison's International Medicine

Part of the brain affected:

Part of the brain affected Left (Dominant) Hemisphere Stroke: Common Pattern Aphasia , Difficulty reading, writing, or calculating Majority of right handed and most left handed patients have dominance for speech and language located in the left hemisphere Left hemisphere infarction is characterized by aphasia (both motor [Broca’s] and sensory [Wernicke’s]) and apraxia Right Hemiparesis Right-sided sensory loss Right visual field defect Poor right conjugate gaze 29 Reference- Harrison's International Medicine

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Right (Non-dominant) Hemisphere Stroke: Common Pattern Less predictable syndromes Left Hemiparesis Left-sided sensory loss Poor left conjugate gaze Dysarthria Attention defects: extinction and neglect Spatial disorientation Behavioral changes: acute confusion and delirium Defect of left visual field 30 Reference- Harrison's International Medicine

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Stroke Syndromes: Classification:

Stroke Syndromes: Classification 34 Reference- Harrison's International Medicine

Vascular Anatomy:

Vascular Anatomy . 35 Reference- Harrison's International Medicine

Cerebral Blood Supply:

Cerebral Blood Supply Anterior Circulation From carotid system Supplies 80% of brain Posterior Circulation From vertebral system Supplies 20% of brain 36 Reference- Harrison's International Medicine

Internal Carotid Artery:

Internal Carotid Artery CA arises from the innominate artery on the right and aortic arch on the left. At level of upper neck CA branches into internal and external the internal carotid artery terminates into the middle (MCA) and anterior (ACA) cerebral arteries 37 Reference- Harrison's International Medicine

Major Vessels:

Major Vessels 38 Reference- Harrison's International Medicine

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The ACA is divided into two segments: the precommunal (A1) which connects the internal carotid artery to the anterior communicating artery the postcommunal (A2) segment - distal to the anterior communicating artery . The A1 segment gives rise to several deep penetrating branches that supply the anterior limb of the internal capsule, the anterior perforate substance, amygdala, anterior hypothalamus, and the inferior part of the head of the caudate nucleus. A2 segment - Supplies basal and medial aspects of the cerebral hemispheres, extends to anterior two thirds of parietal lobe. 40 Reference- Harrison's International Medicine

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Anterior Cerebral Artery Syndrome:

Anterior Cerebral Artery Syndrome Signs and symptoms Structures involved Paralysis of opposite foot and leg A lesser degree of paresis of opposite arm Cortical sensory loss over toes, foot, and leg a Urinary incontinence Contralateral grasp reflex, sucking reflex Abulia (akinetic mutism), slowness, intermittent interruption, lack of spontaneity, whispering, distraction to sights and sounds Impairment of gait and stance (gait apraxia) Dyspraxia of left limbs Motor leg area Arm area of cortex or fibers descending to corona radiata Sensory area for foot and leg Sensorimotor area in paracentral lobule Medial surface of the posterior frontal lobe; likely supplemental motor area probably cingulate gyrus and medial inferior portion of frontal, parietal, and temporal lobes Frontal cortex near leg motor area Corpus callosum 43 Reference- Harrison's International Medicine

Middle Cerebral Artery:

Middle Cerebral Artery MCA supply the lateral surface of the hemisphere except for (1) frontal pole and a strip along the superomedial border of the frontal and parietal lobes supplied by the ACA (2) lower temporal and occipital pole convolutions supplied by PCA The proximal MCA (M1 segment) gives rise to penetrating branches (lenticulostriate arteries) - supply the putamen, outer globus pallidus, posterior limb of the internal capsule, the adjacent corona radiata, caudate nucleus . 44 Reference- Harrison's International Medicine

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In the sylvian fissure, the MCA divides into superior and inferior divisions (M2 branches) Branches from the superior division supply the frontal and superior parietal cortex and those of the inferior division Supply the inferior parietal and temporal cortex 45 Reference- Harrison's International Medicine

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If the entire MCA is occluded at its origin contralateral hemiplegia, hemianesthesia, homonymous hemianopia, and gaze preference to the ipsilateral side. Dysarthria is common because of facial weakness. When the dominant hemisphere is involved, global aphasia is present when the nondominant hemisphere is affected, anosognosia, constructional apraxia, and neglect are found . 47 Reference- Harrison's International Medicine

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Partial syndromes due to embolic occlusion of a single branch include hand, or arm and hand, weakness alone or facial weakness with Broca aphasia, with or without arm weakness A combination of sensory disturbance, motor weakness, and Broca’s aphasia suggests that an embolus has occluded the proximal superior division and infarcted large portions of the frontal and parietal cortices . Wernicke's aphasia without weakness – involvement of the inferior division of the MCA supplying the posterior part (temporal cortex) of the dominant hemisphere Hemineglect or spatial agnosia without weakness indicates – involvement of inferior division of the MCA in the nondominant hemisphere 48 Reference- Harrison's International Medicine

Middle cerebral artery syndrome:

Middle cerebral artery syndrome Signs and symptoms: Structures involved Paralysis of the contralateral face, arm, and leg; sensory impairment over the same area : Somatic motor area for face and arm and the fibers descending from the leg area to enter the corona radiata and corresponding somatic sensory system Motor aphasia: Motor speech area of the dominant hemisphere aphasia, word deafness, anomia, jargon speech, sensory agraphia, acalculia, alexia, finger agnosia, right-left confusion (the last four comprise the Gerstmann syndrome): Central, suprasylvian speech area and parietooccipital cortex of the dominant hemisphere 49 Reference- Harrison's International Medicine

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Anosognosia , unilateral neglect, agnosia for the left half of external space, dressing "apraxia," constructional "apraxia," distortion of visual coordinates, inaccurate localization in the half field, impaired ability to judge distance, upside-down reading, visual illusions: Nondominant parietal lobe Homonymous hemianopia: Optic radiation deep to second temporal convolution Paralysis of conjugate gaze to the opposite side: Frontal eye field 50 Reference- Harrison's International Medicine

Anterior Choroidal Artery:

Anterior Choroidal Artery This artery arises from the internal carotid artery and supplies the posterior limb of the internal capsule and the white matter posterolateral to it The complete syndrome of anterior choroidal artery occlusion consists of contralateral hemiplegia, hemianesthesia and homonymous hemianopia. Since this territory is also supplied by penetrating vessels of the proximal MCA and the posterior communicating and posterior choroidal arteries, minimal deficits may occur, and patients frequently recover substantially. 51 Reference- Harrison's International Medicine

Internal Carotid Artery:

Internal Carotid Artery With a competent circle of Willis, occlusion may go unnoticed. If the thrombus propagates up the internal carotid artery into the MCA or embolizes it, symptoms are identical to proximal MCA occlusion. When the origins of both the ACA and MCA are occluded at the top of the carotid artery, abulia or stupor occurs with hemiplegia, hemianesthesia, and aphasia or anosognosia. 52 Reference- Harrison's International Medicine

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In addition to supplying the ipsilateral brain, the internal carotid artery perfuses the optic nerve and retina via the ophthalmic artery. In 25% of symptomatic internal carotid disease, recurrent transient monocular blindness (amaurosis fugax) warns of the lesion. 53 Reference- Harrison's International Medicine

Posterior Circulation/ Vertebrobasilar System:

Posterior Circulation/ Vertebrobasilar System 2 Vertebral arteries  basilar artery  posterior cerebral arteries 54 Reference- Harrison's International Medicine

Posterior Cerebral Artery:

Posterior Cerebral Artery In 75% of cases, both PCAs arise from bifurcation of basilar artery; in 20%, one has its origin from ipsilateral internal carotid artery; in 5%, both originate from respective ipsilateral ICA Two clinical syndromes are commonly observed with occlusion of the PCA: (1) P1 syndrome : midbrain, subthalamic, and thalamic signs, due to disease of the Proximal P1 segment of the PCA or its penetrating branches (thalamogeniculate, posterior choroidal ) (2) P2 syndrome : cortical temporal & occipital lobe signs, due to occlusion of the P2 segment distal to the junction of the PCA with the posterior communicating artery. 55 Reference- Harrison's International Medicine

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P1 Syndromes Infarction usually occurs in the ipsilateral subthalamus and medial thalamus and in the ipsilateral cerebral peduncle and midbrain. A third nerve palsy with contralateral ataxia (Claude's syndrome) or with contralateral hemiplegia (Weber's syndrome) may result. ataxia - the red nucleus or dentatorubrothalamic tract contralateral hemiballismus - subthalamic nucleus Extensive infarction in the midbrain and subthalamus occurring with bilateral proximal PCA occlusion presents as coma, unreactive pupils, bilateral pyramidal signs, and decerebrate rigidity. Occlusion of the penetrating branches of thalamic and thalamogeniculate arteries produces less extensive thalamic & thalamocapsular lacunar syndromes. The thalamic Déjérine-Roussy syndrome consists of contralateral hemisensory loss followed later by an agonizing, searing or burning pain in the affected areas. 57 Reference- Harrison's International Medicine

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P2 Syndromes Occlusion of the distal PCA causes infarction of the medial temporal and occipital lobes. Contralateral homonymous hemianopia with macula sparing is the usual manifestation. If the visual association areas are spared and only the calcarine cortex is involved, the patient may be aware of visual defects. Medial temporal lobe and hippocampal involvement may cause an acute disturbance in memory, particularly if it occurs in the dominant hemisphere. If the dominant hemisphere is affected and the infarct extends to involve the splenium of the corpus callosum, the patient may demonstrate alexia without agraphia. Visual agnosia for faces, objects, mathematical symbols, and colors and anomia with paraphasic errors may also. Occlusion of the posterior cerebral artery can produce visual hallucinations of brightly colored scenes and objects 58 Reference- Harrison's International Medicine

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Bilateral infarction in the distal PCAs produces cortical blindness (blindness with preserved pupillary light reaction). The patient is often unaware of the blindness or may even deny it (Anton's syndrome). Patients may experience persistence of a visual image for several minutes despite gazing at another scene (palinopsia) or an inability to synthesize the whole of an image (asimultanagnosia). Embolic occlusion of the top of the basilar artery can produce any or all of the central or peripheral territory symptoms. The hallmark is the sudden onset of bilateral signs, including pupillary asymmetry or lack of reaction to light 59 Reference- Harrison's International Medicine

Vertebral and Posterior Inferior Cerebellar Arteries:

Vertebral and Posterior Inferior Cerebellar Arteries The vertebral artery, which arises from the innominate artery on the right and the subclavian artery on the left, consists of four segments. V1 extends from its origin to its entrance into the 6 th transverse vertebral foramen. V2 traverses the vertebral foramina from C6 to C2. V3 passes through the transverse foramen and circles around the arch of the atlas to pierce the dura at the foramen magnum. V4 segment courses upward to join the other vertebral artery to form the basilar artery; only the fourth segment gives rise to branches that supply the brainstem and cerebellum. The posterior inferior cerebellar artery (PICA) in its proximal segment supplies the lateral medulla and, in its distal branches, the inferior surface of the cerebellum. 60 Reference- Harrison's International Medicine

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If the subclavian artery is occluded proximal to the origin of the vertebral artery, there is a reversal in the direction of blood flow in the ipsilateral vertebral artery. Exercise of the ipsilateral arm may increase demand on vertebral flow, producing posterior circulation TIAs, or "subclavian steal.” 61 Reference- Harrison's International Medicine

Basilar Artery:

Basilar Artery Branches of the basilar artery supply the base of the pons and superior cerebellum and fall into three groups: Paramedian , 7–10 in number, which supply a wedge of pons on either side of the midline short circumferential, 5–7 in number, that supply the lateral two-thirds of the pons and middle and superior cerebellar peduncles bilateral long circumferential (superior cerebellar and anterior inferior cerebellar arteries), which course around the pons to supply the cerebellar hemispheres. 62 Reference- Harrison's International Medicine

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On side of lesion Paralysis with atrophy of one-half half the tongue: Ipsilateral twelfth nerve On side opposite to lesion Paralysis of arm and leg, sparing face; impaired tactile and proprioceptive sense over one-half the body: Contralateral pyramidal tract and medial lemniscus Medial medullary syndrome (occlusion of vertebral artery or of branch of vertebral or lower basilar artery) 63

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On side of lesion Pain, numbness, impaired sensation over one-half the face: Descending tract and nucleus fifth nerve Ataxia of limbs, falling to side of lesion: restiform body, cerebellar hemisphere, cerebellar fibers, spinocerebellar tract Nystagmus , diplopia , vertigo, nausea, vomiting: Vestibular nucleus Horner's syndrome ( miosis , ptosis , decreased sweating): Descending sympathetic tract Lateral medullary syndrome (occlusion of any of the five vessels may be responsible –vertebral, posterior inferior cerebellar, superior, middle or inferior lateral medullary arteries) 64 Reference- Harrison's International Medicine

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Dysphagia, hoarseness, paralysis of palate, paralysis of vocal cord, diminished gag reflex: Issuing fibers ninth and tenth nerves Loss of taste: Nucleus and tractus solitarius Numbness of ipsilateral arm, trunk, or leg: Cuneate and gracile nuclei Weakness of lower face: Genuflected upper motor neuron fibers to ipsilateral facial nucleus On side opposite to lesion Impaired pain and thermal sense over half the body, sometimes face: Spinothalamic tract 65 Reference- Harrison's International Medicine

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Total Unilateral medullary syndrome (occlusion of vertebral artery) Combination of medial and lateral syndromes Lateral pontomedullary syndrome (occlusion of vertebral artery) Combination of lateral medullary and lateral inferior pontine syndrome Basilar artery syndrome Combination of brainstem syndromes plus those arising in PCA distribution Bilateral long tract signs (sensory and motor; cerebellar and peripheral cranial nerve abnormalities): Bilateral long tract; cerebellar and peripheral cranial nerves Paralysis or weakness of all extremities, plus all bulbar musculature: Corticobulbar and corticospinal tracts bilaterally 66 Reference- Harrison's International Medicine

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On side of lesion Cerebellar ataxia (probably): Superior and/or middle cerebellar peduncle Internuclear ophthalmoplegia: Medial longitudinal fasciculus Myoclonic syndrome, palate, pharynx, vocal cords, respiratory apparatus, face, oculomotor apparatus, etc.: central tegmental bundle, dentate projection, inferior olivary nucleus On side opposite lesion Paralysis of face, arm, and leg: Corticobulbar and corticospinal tract Rarely touch, vibration, and position are affected: Medial lemniscus Medial Superior pontine syndrome (paramedian branches of upper basilar artery) 67

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On side of lesion Ataxia of limbs and gait, falling to side of lesion: Middle and superior cerebellar peduncles, superior surface of cerebellum, dentate nucleus Dizziness, nausea, vomiting; horizontal nystagmus: Vestibular nucleus Paresis of conjugate gaze (ipsilateral): Pontine contralateral gaze L ateral superior pontine syndrome (Syndrome of superior cerebellar artery) 68 Reference- Harrison's International Medicine

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Miosis, ptosis, decreased sweating over face (Horner's syndrome): Descending sympathetic fibers Tremor: Dentate nucleus, superior cerebellar peduncle On side opposite lesion Impaired pain and thermal sense on face, limbs, and trunk: Spinothalamic tract Impaired touch, vibration, and position sense : Medial lemniscus (lateral portion) 69 Reference- Harrison's International Medicine

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On side of lesion Ataxia of limbs and gait (more prominent in bilateral involvement): Pontine nuclei On side opposite lesion Paralysis of face, arm, and leg: Corticobulbar and corticospinal tract Variable impaired touch and proprioception when lesion extends posteriorly: Medial lemniscus Medial midpontine syndrome (paramedian branch of midbasilar artery) 70

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On side of lesion Ataxia of limbs: Middle cerebellar peduncle Paralysis of muscles of mastication: Motor fibers or nucleus of fifth nerve Impaired sensation over side of face: Sensory fibers or nucleus of fifth nerve On side opposite lesion Impaired pain and thermal sense on limbs and trunk: Spinothalamic tract Lateral midpontine syndrome (Short circumferential artery) 71

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On side of lesion Paralysis of conjugate gaze to side of lesion (preservation of convergence): Center for conjugate lateral gaze Nystagmus: Vestibular nucleus Ataxia of limbs and gait: Likely middle cerebellar peduncle Diplopia on lateral gaze: Abducens nerve On side opposite lesion Paralysis of face, arm, and leg: Corticobulbar and corticospinal tract in lower pons Impaired tactile and proprioceptive sense over half of the body: Medial lemniscus Medial inferior pontine syndrome (occlusion of paramedian branch of basilar artery) 72

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On side of lesion Horizontal and vertical nystagmus, vertigo, nausea, vomiting, oscillopsia: Vestibular nerve or nucleus Facial paralysis: Seventh nerve Paralysis of conjugate gaze to side of lesion: Center for conjugate lateral gaze Deafness, tinnitus: Auditory nerve or cochlear nucleus Ataxia: Middle cerebellar peduncle and cerebellar hemisphere Impaired sensation over face: Descending tract and nucleus fifth nerve On side opposite lesion Impaired pain and thermal sense over one-half the body (may include face): Spinothalamic tract Lateral inferior pontine syndrome (occlusion of anterior inferior cerebellar artery) 73 Reference- Harrison's International Medicine

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On side of lesion Eye "down and out" secondary to unopposed action of fourth and sixth cranial nerves, with dilated and unresponsive pupil: Third nerve fibers On side opposite lesion Paralysis of face, arm, and leg: Corticobulbar and corticospinal tract descending in crus cerebri Medial midbrain syndrome (paramedian branches of upper basilar and proximal posterior cerebral arteries) 74 Reference- Harrison's International Medicine

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On side of lesion Eye "down and out" secondary to unopposed action of fourth and sixth cranial nerves, with dilated and unresponsive pupil: Third nerve fibers and/or third nerve nucleus On side opposite lesion Hemiataxia , hyperkinesias, tremor: Red nucleus, dentatorubrothalamic pathway Lateral midbrain syndrome (syndrome of small penetrating arteries arising from posterior cerebral artery) 75 Reference- Harrison's International Medicine

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Brain Stem Stroke: Common Pattern Hemiparesis or tetraparesis Sensory loss Diplopia Facial numbness Facial weakness (lower motor neurone) Nystagmus, vertigo Dysphagia, Dysarthria Ataxia, hiccups, vomiting Horner's syndrome Altered consciousness Crossed signs 76 Reference- Harrison's International Medicine

Lacunar Infarct:

Lacunar Infarct Small penetrating branches HT, DM, Atherosclerosis Pure motor hemiplegia – Lenticulostriate territory Pure sensory stroke – Lat. Thalamus Clumsy hand dysarthria ataxic hemiparesis – ataxia 77 Reference- Harrison's International Medicine

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Watershed Infarction:

Watershed Infarction occurs in vulnerable areas supplied by distal distribution cerebral arteries during periods of hypotension infarction between the anterior and middle cerebral arteries presents with hemiparesis and hemianesthesia, predominantly in the leg dominant hemisphere infarctions: decrease in verbal ability with preserved comprehension Infarction involving the posterior watershed area presents with homonymous hemianopia +/- hypoesthesia in the face and legs 79 Reference- Harrison's International Medicine

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