Stroke Syndromes and Localization Ozcan Ozdemir, MD Clinical Stroke Fellow, LHSC

Stroke Syndromes and Localization Ozcan Ozdemir, MD Clinical Stroke Fellow, LHSC

Stroke localization and syndromes

Stroke localization and syndromes

Objective Stroke definition, symptoms Stroke mimics Stroke syndromes

Objective Stroke definition, symptoms Stroke mimics Stroke syndromes

Stroke: An Operational Definition

Stroke: An Operational Definition

A clinical syndrome.

Focal neurological deficits due to presumed vascular disturbance within the central nervous system that evolve over a short period of time (seconds to hours) and last more than 24 hours (1 hr).

A clinical syndrome.

Focal neurological deficits due to presumed vascular disturbance within the central nervous system that evolve over a short period of time (seconds to hours) and last more than 24 hours (1 hr).

Case Study Case Study

82 year old man brought to hospital after he was found to be in a confused state and wandering the hallway of his apartment complex. He gave the wrong date and thought he was in a park Neurological examination did not reveal any visual field cut, weakness, or inccordination.

82 year old man brought to hospital after he was found to be in a confused state and wandering the hallway of his apartment complex. He gave the wrong date and thought he was in a park Neurological examination did not reveal any visual field cut, weakness, or inccordination.

Case Study Case Study

Fever 38.5°, abnormal lung examination Determination: Not a stroke.

Actual diagnosis: Pneumonia with septic encephalopathy

Fever 38.5°, abnormal lung examination Determination: Not a stroke.

Actual diagnosis: Pneumonia with septic encephalopathy

70 years old gentelman with unremarkable vascular history presented with sudden onset of speech disturbance and right arm weakness (Symptom onset 1 hour)/ Neurological examination revealed right arm weakness and expressive aphasia His son noticed that his right arm has been shaking for almost 1 week

Major stroke syndromes I Major stroke syndromes I Middle cerebral artery (MCA)

contralateral hemiparesis contralateral sensory loss

arm and face > leg contralateral homonymous hemianopsia gaze preference toward the side of the lesion receptive or expressive aphasia (dominant) agnosia (non-dominant)

Middle cerebral artery (MCA) contralateral hemiparesis contralateral sensory loss

arm and face > leg contralateral homonymous hemianopsia gaze preference toward the side of the lesion receptive or expressive aphasia (dominant) agnosia (non-dominant)

Anterior cerebral artery (ACA)

contralateral leg weakness and sensory loss Bilateral: altered mental status, abulia, akinetic mutism

Anterior cerebral artery (ACA)

contralateral leg weakness and sensory loss Bilateral: altered mental status, abulia, akinetic mutism

Major stroke syndromes II Major stroke syndromes II Posterior cerebral artery (PCA)

contralateral homonymous hemianopsia cortical blindness visual agnosia altered mental status impaired memory

Posterior cerebral artery (PCA)

contralateral homonymous hemianopsia cortical blindness visual agnosia altered mental status impaired memory

Vertebrobasilar artery

visual field deficits diplopia nystagmus dysphagia dysarthria vertigo ataxia weakness and sensory loss bilateral symptoms/signs decreased LOC

Is the patient having a stroke? Is the patient having a stroke? Goldstein et al reviewed 1994 report regarding the accuracy and reliability of symptoms and findings for the evaluation of patients with suspected stroke and TIA. The presence of acute facial paresis, arm drift or abnormal speech increases the likehood of stroke Symptoms associated with high agreement for the diagnosis of stroke and TIA vs non-vascular event:

Sudden change in speech, visual loss, diplopia, paralysis or weaknes, numbness or tingling

Goldstein et al reviewed 1994 report regarding the accuracy and reliability of symptoms and findings for the evaluation of patients with suspected stroke and TIA. The presence of acute facial paresis, arm drift or abnormal speech increases the likehood of stroke Symptoms associated with high agreement for the diagnosis of stroke and TIA vs non-vascular event:

Sudden change in speech, visual loss, diplopia, paralysis or weaknes, numbness or tingling

JAMA 2005;19:2931-2401

Misdiagnosis of stroke Norris Lancet 1982;1:1523

Misdiagnosis of stroke Norris Lancet 1982;1:1523

821 patients consecutively admitted to a stroke unit from ER Evaluators – Interns then neurology Initial studies - History and physical Further studies – CT head, LP, EEG

821 patients consecutively admitted to a stroke unit from ER Evaluators – Interns then neurology Initial studies - History and physical Further studies – CT head, LP, EEG

Misdiagnosis of stroke Norris Lancet 1982;1:1523

Misdiagnosis of stroke Norris Lancet 1982;1:1523

Stroke mimic rate 13% Post-ictal state, non-convulsive status (5%) Confusional state: metabolic, psychogenic, drugs, alcohol Subdural hematoma CNS tumor Radial-nerve palsy Vertigo Encephalitis Cardiac failure Multiple sclerosis

Stroke mimic rate 13% Post-ictal state, non-convulsive status (5%) Confusional state: metabolic, psychogenic, drugs, alcohol Subdural hematoma CNS tumor Radial-nerve palsy Vertigo Encephalitis Cardiac failure Multiple sclerosis

Conditions that mimic stroke in the ER Libman et al. Arch Neurol 1995; 52:1119-22

Conditions that mimic stroke in the ER Libman et al. Arch Neurol 1995; 52:1119-22

411 consecutive patients presenting to ER with initial diagnosis of stroke

75% made by ER physician Diagnosed as “Mimic” or “True stroke” by history and physical alone

Stroke or hemorrhage = “true” stroke Mimics: 78 patients (19%)

411 consecutive patients presenting to ER with initial diagnosis of stroke

75% made by ER physician Diagnosed as “Mimic” or “True stroke” by history and physical alone

Stroke or hemorrhage = “true” stroke Mimics: 78 patients (19%)

Seizure with post-ictal deficit (17%) Systemic infection (17%) Brain tumor (15%) Toxic-Metabolic disturbance (13%) Positional vertigo Cardiac Syncope Trauma Subdural hematoma Herpes encephalitis

Seizure with post-ictal deficit (17%) Systemic infection (17%) Brain tumor (15%) Toxic-Metabolic disturbance (13%) Positional vertigo Cardiac Syncope Trauma Subdural hematoma Herpes encephalitis

Transient global amnesia Dementia Multiple Sclerosis Demyelinating disease Cervical spine fracture Myasthenia Gravis Parkinsonism Hypertensive encephalopathy Conversion disorder

Transient global amnesia Dementia Multiple Sclerosis Demyelinating disease Cervical spine fracture Myasthenia Gravis Parkinsonism Hypertensive encephalopathy Conversion disorder

Conditions that mimic stroke in the ER Libman et al. Arch Neurol 1995; 52:1119-22

Mimics of acute ischemic stroke Mimics of acute ischemic stroke Seizures

Post-ictal “Todd’s paresis” Non-convulsive status epilepticus

Vascular lesions Intracerebral hemorrhage Extra-axial hemorrhage (EDH, SDH) Subarachnoid hemorrhage Venous sinus thrombosis

Mass lesions Tumors or abcess

Toxic / Metabolic Hypo-/hyper-glycemia, hyponatremia, hypercalcemia Drug intoxication

Seizures Post-ictal “Todd’s paresis” Non-convulsive status epilepticus

Vascular lesions Intracerebral hemorrhage Extra-axial hemorrhage (EDH, SDH) Subarachnoid hemorrhage Venous sinus thrombosis

Mass lesions Tumors or abcess

Toxic / Metabolic Hypo-/hyper-glycemia, hyponatremia, hypercalcemia Drug intoxication

Infections Encephalitis, meningitis Systemic

Migraine with aura (complicated) Hypertensive encephalopathy Multiple sclerosis Transient global amnesia Positional vertigo Psychiatric (‘conversion disorder’)

Infections Encephalitis, meningitis Systemic

Migraine with aura (complicated) Hypertensive encephalopathy Multiple sclerosis Transient global amnesia Positional vertigo Psychiatric (‘conversion disorder’)

Clues to non-ischemic etiology Clues to non-ischemic etiology Subacute History of trauma, epilepsy, malignancy, diabetes Prominent headache

Migraine, ICH, mass lesion Positive visual and/or sensory symptoms (“aura”)

Loss of consciousness at onset (ictal) Fluctuating LOC, incontinence, tongue biting Rapidly improving LOC & deficits Early focal seizures unusual with ischemic stroke

Inconsistent findings Lack of objective signs such as reflex changes or does not fit an anatomical pattern / vascular territory

Subacute History of trauma, epilepsy, malignancy, diabetes Prominent headache

Migraine, ICH, mass lesion Positive visual and/or sensory symptoms (“aura”)

Loss of consciousness at onset (ictal) Fluctuating LOC, incontinence, tongue biting Rapidly improving LOC & deficits Early focal seizures unusual with ischemic stroke

Inconsistent findings Lack of objective signs such as reflex changes or does not fit an anatomical pattern / vascular territory

Misdiagnosis of Stroke in tPA-Treated Patients Misdiagnosis of Stroke in tPA-Treated Patients

6/151 patients had a final diagnosis other than acute ischemic stroke

4 conversion disorder 1 complex migraine Todd`s paralysis

No ICH was seen after thrombolysis

6/151 patients had a final diagnosis other than acute ischemic stroke

4 conversion disorder 1 complex migraine Todd`s paralysis

No ICH was seen after thrombolysis

A.Scott et al. Annals of Emergency Medicine

Useful Questions?? Useful Questions?? Vomiting is more common in ICH (48-67%), SAH (48-68%)

and posterior circulation strokes (29% vs 2% ant circulation) Lacunar stroke 1-2%

Headache ICH 33-41% SAH 78-87% Lacunar stroke 3-7% Embolic 9-18% and thrombotic stroke 11-17% Post circulation stroke 40% Decreased consciousness ICH 39-57% SAH 48-68% Ischemic stroke 2-29% Lacunar 2-3% Post-circulation 18%

Vomiting is more common in ICH (48-67%), SAH (48-68%) and posterior circulation strokes (29% vs 2% ant circulation) Lacunar stroke 1-2%

Headache ICH 33-41% SAH 78-87% Lacunar stroke 3-7% Embolic 9-18% and thrombotic stroke 11-17% Post circulation stroke 40% Decreased consciousness ICH 39-57% SAH 48-68% Ischemic stroke 2-29% Lacunar 2-3% Post-circulation 18%

Time of onset Preceeding palpitation Activity at the onset of symptoms (majority on daily activity) Temporal course and progression of findings

Fluctuations??? Stepwise??? Gradual?? Max at onset SAH 64-84%, Lacune 38-54%, Embolic 79-82% Thrombotic 40-66%, ICH 34-44% Stepwise /slutter Thrombosis 32-34%, Lacune 28-30%, Others <15% Gradual ICH 51-63%

Time of onset Preceeding palpitation Activity at the onset of symptoms (majority on daily activity) Temporal course and progression of findings

Fluctuations??? Stepwise??? Gradual?? Max at onset SAH 64-84%, Lacune 38-54%, Embolic 79-82% Thrombotic 40-66%, ICH 34-44% Stepwise /slutter Thrombosis 32-34%, Lacune 28-30%, Others <15% Gradual ICH 51-63%

65 years old lady, PMH of diabetes and hypertension presented with acute onset left sided facial drop, left upper and lower extremity paralysis at 8.00 am (Woke up normally).

No headache and neck pain, vomiting, nausea, duble vision, balance problem, visual disturbance, speech disturbance sensory symptoms. No fluctuations were Observed. She was aware of her deficit. Neurological exam: BP 176/89 Alert, oriented. Left facial drop. Left upper extr power 1/5 (prox, distal) , left lower extr 1/5 (prox, distal). Upgoing toes on the left.

Lacunar syndromes Lacunar syndromes

The term of lacuna was primarly used in pathological studies (1838) CM Fisher described several syndromes

Pure motor hemiplegia Pure sensory stroke Homolateral ataxia and crural paresis Dysartria-clumsy hand syndrome Sensory-motor stroke (Proposed later)

The term of lacuna was primarly used in pathological studies (1838) CM Fisher described several syndromes

Pure motor hemiplegia Pure sensory stroke Homolateral ataxia and crural paresis Dysartria-clumsy hand syndrome Sensory-motor stroke (Proposed later)

Lacune refers to a small deep infarct attributable to a primary arterial disease that involves a penetrating branch of a large cerebral artery. Vessels are 100-400 µm in size and infarction could be as large as 15 mm. Putamen, thalamus, internal capsule, pons, corona radiata

Lacune refers to a small deep infarct attributable to a primary arterial disease that involves a penetrating branch of a large cerebral artery. Vessels are 100-400 µm in size and infarction could be as large as 15 mm. Putamen, thalamus, internal capsule, pons, corona radiata

Pure motor hemiplegia Pure motor hemiplegia A paralysis complete or incomplete of the face, arm and the leg on one side unaccompanied by sensory signs, visual field defect, dyphasia, agnosia and apraxia.

A paralysis complete or incomplete of the face, arm and the leg on one side unaccompanied by sensory signs, visual field defect, dyphasia, agnosia and apraxia.

PMH ranged from 7-9% in stroke registries. 2/3 cases, lacunes are in internal capsule Pons (28%), corona radiata, cerebral peduncle and the medullary pyramid Pontine versus internal capsule?????

Cannot be distinguished Transient dysartria, gait ataxia, vertigo is more

common in pontine origin PMH

PMH ranged from 7-9% in stroke registries. 2/3 cases, lacunes are in internal capsule Pons (28%), corona radiata, cerebral peduncle and the medullary pyramid Pontine versus internal capsule?????

Cannot be distinguished Transient dysartria, gait ataxia, vertigo is more

common in pontine origin PMH

Pure sensory stroke Pure sensory stroke 6% of LCAS are sensory strokes. Original paper of Fisher suggested objective sensory loss However subjective sensory symptoms in the absence of objective signs were reported by CM Fisher Complete or incomplete sensory syndromes Localization: Thalamus (thalamus or thalamocortical pathways, anterior limb internal capsule Non-lacunar lesions were found in 0-3% in several studies

6% of LCAS are sensory strokes. Original paper of Fisher suggested objective sensory loss However subjective sensory symptoms in the absence of objective signs were reported by CM Fisher Complete or incomplete sensory syndromes Localization: Thalamus (thalamus or thalamocortical pathways, anterior limb internal capsule Non-lacunar lesions were found in 0-3% in several studies

Sensory- motor stroke Sensory- motor stroke Originally is not included in LACS Several autopsy cases were reported and SMS was described SMS is the second most common lacunar syndromes Location: Thalamus, internal capsule, corona radiata

Originally is not included in LACS Several autopsy cases were reported and SMS was described SMS is the second most common lacunar syndromes Location: Thalamus, internal capsule, corona radiata

Dysartria-clumsy hand syndrome Ataxic hemiparesis

Dysartria-clumsy hand syndrome Ataxic hemiparesis

Dysartria is associated with a LACS in 53% of cases The dysartria and the ataxia of the upper limb is the prominent component Upper neuron type facial paresis and lingual paresis can also accompany Internal capsule, pons , corona radiata 94% of patients supported lacunar hypothesis

Ataxic hemiparesis Original description of AH was homolateral ataxia and crural paresis The syndrome of AH has both cerebellar and pyramidal elements. Ataxic hemiparesis can be due to internal capsule, corona radiata, pons involvement.

Dysartria is associated with a LACS in 53% of cases The dysartria and the ataxia of the upper limb is the prominent component Upper neuron type facial paresis and lingual paresis can also accompany Internal capsule, pons , corona radiata 94% of patients supported lacunar hypothesis

Ataxic hemiparesis Original description of AH was homolateral ataxia and crural paresis The syndrome of AH has both cerebellar and pyramidal elements. Ataxic hemiparesis can be due to internal capsule, corona radiata, pons involvement.

66 years old gentelman, R handed, presented with acute onset of slurred speech and clumsiness on left hand.

Denied headache, double vision, visual disturbance, vertigo, speech disturbance, vomiting and nausea.

Neurological exam: Dysartria, left hand impaired alternating movements (slowness of movements).

66 years old gentelman, R handed, presented with acute onset of slurred speech and clumsiness on left hand.

Denied headache, double vision, visual disturbance, vertigo, speech disturbance, vomiting and nausea.

Neurological exam: Dysartria, left hand impaired alternating movements (slowness of movements).

MRA is completely normal

Some points about lacunar syndromes Some points about lacunar syndromes 5% of pure motor presentation could be non-ischemic stroke origin with acute onset of deficits. LACS is not synonymous with the presence of hypertensive arteriopathy. Complete investigations must be performed on all patients presenting with lacunar syndromes

5% of pure motor presentation could be non-ischemic stroke origin with acute onset of deficits. LACS is not synonymous with the presence of hypertensive arteriopathy. Complete investigations must be performed on all patients presenting with lacunar syndromes

76 years old gentelman with a history of hypertension (10 years) presented with 4 fluctuating episodes of right sided face, upper and lower extremity weakness followed by tinhling sensation on right side of his face, arm and leg. Between episodes he was completely normal. Finally he had right facial drop, right pronator drift sign and right lower extremity was slightly weaker. Otherwise normal.

MRA was completely normal

Possible mechanisms In situ atheromatous plaque Large vessel atheroma lipping over the penetrator origins Vasospasm Intermittent metabolic dysfunction (Increase in lactate, spreading depression

like event, peri-infarct depolarizations)

Possible mechanisms In situ atheromatous plaque Large vessel atheroma lipping over the penetrator origins Vasospasm Intermittent metabolic dysfunction (Increase in lactate, spreading depression

like event, peri-infarct depolarizations)

Donnan 1980 described the capsular warning syndrome. Stereotypic nature of the TIAs preceding lacunar infarction. Brief bursts of hemiplegia, hemisensory loss or other expressions of LACS and complete resolution between events Basal ganglia, pons, corona radiata and other adjacent motor pathways

Donnan 1980 described the capsular warning syndrome. Stereotypic nature of the TIAs preceding lacunar infarction. Brief bursts of hemiplegia, hemisensory loss or other expressions of LACS and complete resolution between events Basal ganglia, pons, corona radiata and other adjacent motor pathways

Capsular warning sign: crescendo subcortical transient ischemic attacks

Capsular warning sign: crescendo subcortical transient ischemic attacks

Striocapsular infarcts Striocapsular infarcts Defined as large 20 mm> subcortical infarcts in the territory of lentriculostriate arteries. There are usually 2 medial and 4-5 lateral LSAs. LSAs supply lateral globus pallidus, medial putamen, putamen, external capsule, head of caudate, the anterior limb of the internal capsule, anterior party of the periventricular corona radiata LSAs are end-arteries and arise with acute angle from main trunk M1 Their presentation, prognosis and pathogenesis are different

Defined as large 20 mm> subcortical infarcts in the territory of lentriculostriate arteries. There are usually 2 medial and 4-5 lateral LSAs. LSAs supply lateral globus pallidus, medial putamen, putamen, external capsule, head of caudate, the anterior limb of the internal capsule, anterior party of the periventricular corona radiata LSAs are end-arteries and arise with acute angle from main trunk M1 Their presentation, prognosis and pathogenesis are different

24 years old gentelman , R handed , woke up normally and went to bathroom, Developed sudden onset of right sided paralysis and speech arrest. He could express himself. (8.30 am). 9.30 his neurological examination revelaed expressive aphasia. His comprehension was 80% intact. Repetition was impaired. Motor power on right upper extremity was 3/5 and 4/5 in lower extremity. Sensory Examination showed decreased pinprick sensation on right-sided face, arm and leg. No gaze palsy, visual cut was detected. IV tpa was given at 10.00 am. Major improvement was seen. Left with right sided hemiparesis (arm>leg)+decreased Pinprick sensation on right side of his body (face, arm and leg, trunk was not involved)

Clinical presentation Clinical presentation Preceeding TIAs in the ipsilateral carotid artery is reported in 10-12% Facio-bracial weakness 99% 60% neglect and aphasia Recovery

Full 38% Absent 29%

Preceeding TIAs in the ipsilateral carotid artery is reported in 10-12% Facio-bracial weakness 99% 60% neglect and aphasia Recovery

Full 38% Absent 29%

Anterior choroidal artery infarcts Anterior choroidal artery infarcts Originates from internal carotid artery First branch of the ICA distal to the posterior communicating artery Supplies optic tract, lateral geniculate body, cerebral pedincule, tip of temporal lobe, choroidal phelexus of lateral ventricule,posterior part of the amygdaloid nucleus, posterior two-thirds of the posterior limb of the internal capsule, globus pallidus Involvement of posterior corona radiata is still a debate Etiology is small vessel disease, cardioembolism, carotid artery atherosclerotic disease

Originates from internal carotid artery First branch of the ICA distal to the posterior communicating artery Supplies optic tract, lateral geniculate body, cerebral pedincule, tip of temporal lobe, choroidal phelexus of lateral ventricule,posterior part of the amygdaloid nucleus, posterior two-thirds of the posterior limb of the internal capsule, globus pallidus Involvement of posterior corona radiata is still a debate Etiology is small vessel disease, cardioembolism, carotid artery atherosclerotic disease

AChA territory infarcts represent between 1%-10% The classical triad consisting of hemiplegia,

hemianesthesia, homonymus hemianopia is rare The most frequent type of presentation is lacunar

syndrome 90% cases have motor hemiparesis with or without sensory deficit. Motor symptoms are due to internal capsule, posterior corona radiata involvement, cerebral peduncule ???? Sensory symptoms are quite variable Ataxic hemiparesis (hypesthetic) is also described Visual field loss

Homonymus hemianopsia Upper quadrantonopia Upper and lower sector anopia (sparing of horizontal meridian occur) Neuropsychological cortical signs

AChA territory infarcts represent between 1%-10% The classical triad consisting of hemiplegia,

hemianesthesia, homonymus hemianopia is rare The most frequent type of presentation is lacunar

syndrome 90% cases have motor hemiparesis with or without sensory deficit. Motor symptoms are due to internal capsule, posterior corona radiata involvement, cerebral peduncule ???? Sensory symptoms are quite variable Ataxic hemiparesis (hypesthetic) is also described Visual field loss

Homonymus hemianopsia Upper quadrantonopia Upper and lower sector anopia (sparing of horizontal meridian occur) Neuropsychological cortical signs

Middle cerebral artery syndromes Middle cerebral artery syndromes According to vascular territories

Main trunk occlusion Upper division syndromes Lower division syndromes Branch occlusion

According to hemisphere side (Right versus left)

According to vascular territories Main trunk occlusion Upper division syndromes Lower division syndromes Branch occlusion

According to hemisphere side (Right versus left)

Hemiplegia and hemiparesis Combined deep and superficial infarction Contralateral hemiplegia, hemianesthesia, homonymus hemianopia, conjugate gaze deviation in the contralateral side Neuropsychological disturbances Aphasia, apraxia, visuospatial neglect, motor impersistence, dressing and constructional apraxia Deep infarction alone Convexity infarctions Faciobracial predominance Opercular and insular infarcts leads to face, oropharynx weakness Distal predominance paresis affects the lower face, fingers, forearm, toes and lower leg

Hemiplegia and hemiparesis Combined deep and superficial infarction Contralateral hemiplegia, hemianesthesia, homonymus hemianopia, conjugate gaze deviation in the contralateral side Neuropsychological disturbances Aphasia, apraxia, visuospatial neglect, motor impersistence, dressing and constructional apraxia Deep infarction alone Convexity infarctions Faciobracial predominance Opercular and insular infarcts leads to face, oropharynx weakness Distal predominance paresis affects the lower face, fingers, forearm, toes and lower leg

MCA superior or anterior division territory infarcts Supplies the frontal, superior parietal lobes Prominent faciobracial deficit Hemisensory loss Conjugate eye deviation Non-dominant hemipshere Visuspatial abnormalities for non-dominant hemisphere Denial of hemiplegia, dysprosodia, motor impersistence, dressing apraxia, constructional apraxia Dominant hemisphere Aphasia, alexia with agraphia Gerstmann`s syndrome (right-left disorientation, finger agnosia, acalculia and dysgraphia)

MCA superior or anterior division territory infarcts Supplies the frontal, superior parietal lobes Prominent faciobracial deficit Hemisensory loss Conjugate eye deviation Non-dominant hemipshere Visuspatial abnormalities for non-dominant hemisphere Denial of hemiplegia, dysprosodia, motor impersistence, dressing apraxia, constructional apraxia Dominant hemisphere Aphasia, alexia with agraphia Gerstmann`s syndrome (right-left disorientation, finger agnosia, acalculia and dysgraphia)

Inferior Division MCA Infarctions Supplies the lateral surface of the temporal lobe and inferior parietal lobule 14% patients have inf division of MCA Usually have no elementary motor or sensory abnormalities They often have a visual field defect Wernicke`s aphasia and conduction aphasia Acute confusional state (right middle temporal gyrus and inf parietal lobe)

Inferior Division MCA Infarctions Supplies the lateral surface of the temporal lobe and inferior parietal lobule 14% patients have inf division of MCA Usually have no elementary motor or sensory abnormalities They often have a visual field defect Wernicke`s aphasia and conduction aphasia Acute confusional state (right middle temporal gyrus and inf parietal lobe)

59 years old gentelman, R handed, PMH of atrial fibrillation and NIDDM presented with left sided weakness (Arm>leg). He was trying to talk however he could not able to vocalize any sound. He also had swallowing diffuculty. Denied headache, double vision, vertigo. NE: Fully alert, oriented. Mute, could not smile or prodrude his tongue. Obey simple and complex commands. Left arm 3/5 power, left lower extremity power was 4/5. Sensory examination was normal. Cortical signs: sensory extinction on left side. No evidenece of anasognosia ,motor impersitence

Major stroke syndromes Major stroke syndromes Posterior cerebral artery (PCA)

contralateral homonymous hemianopsia cortical blindness visual agnosia altered mental status impaired memory Less likely aphasia (anomic, transcortical sensory)

Posterior cerebral artery (PCA)

contralateral homonymous hemianopsia cortical blindness visual agnosia altered mental status impaired memory Less likely aphasia (anomic, transcortical sensory)

Vertebrobasilar artery

visual field deficits diplopia nystagmus dysphagia dysarthria Vertigo and dizziness

(<1% isolated) ataxia weakness and sensory loss bilateral symptoms/signs decreased LOC Hearing loss

Basilary artery occlusive disease Basilary artery occlusive disease Decreased LOC 16% Motor signs

Hemiplegia 44% Tetraparesis/tetraplegia 5%

Cerebellar 43% Vertigo/dizziness 47% Nausea 30% Sensory abnormalities 34% Headache 36% Ocular abnormalities 39% Bulbar/pseudobulbar 64%

Decreased LOC 16% Motor signs

Hemiplegia 44% Tetraparesis/tetraplegia 5%

Cerebellar 43% Vertigo/dizziness 47% Nausea 30% Sensory abnormalities 34% Headache 36% Ocular abnormalities 39% Bulbar/pseudobulbar 64%

A 57 year-old lady, R handed, had transient attack of dizziness and left face tingling sensation that lasted 15 minutes. Awakening next day she felt dizzy as if the room were rocking or wavering like a ship. She leaned to the left when she tried to stand. Her voice was hoarse. She also vomited couple of times and gagged as she tried to swallow water.

A 57 year-old lady, R handed, had transient attack of dizziness and left face tingling sensation that lasted 15 minutes. Awakening next day she felt dizzy as if the room were rocking or wavering like a ship. She leaned to the left when she tried to stand. Her voice was hoarse. She also vomited couple of times and gagged as she tried to swallow water.

NE showed diminished pain and temperature sensation on the left face and right body including limbs. Nystagmus, worse on looking leftward, left ptosis with a smaller pupil. Decreased palatal motion on the left.

Lateral Medullary Syndrome

Isolated lateral medullary syndrome

75 % occurs suddenly

25% non-sudden Headache, vertigo, gait

ataxia occurs earlier Dysphagia, hiccups, sensory

Symptoms occur lately

Very common signs and symptoms (90%) Sensory symptoms and signs (96%) Sensory gradient may occur Several sensory patterns can occur Ipsilat trigeminal Bilateral trigeminal Contralateral trigeminal Isolated limb/body Isolated trigeminal 26 % only have classical pattern 25% (contralat trigeminal-limb/body pattern) Large group (51% bilateral trigeminal) Ventral group (100% contralateral trigeminal) Isolated limb/body sensory symptoms (57%) occur In lateral group

Very common signs and symptoms (90%) Sensory symptoms and signs (96%) Sensory gradient may occur Several sensory patterns can occur Ipsilat trigeminal Bilateral trigeminal Contralateral trigeminal Isolated limb/body Isolated trigeminal 26 % only have classical pattern 25% (contralat trigeminal-limb/body pattern) Large group (51% bilateral trigeminal) Ventral group (100% contralateral trigeminal) Isolated limb/body sensory symptoms (57%) occur In lateral group

Gait ataxia 92% Horner sign 88% Dizziness 92%

Moderately common sign 50-70% Dysphagia Hoarseness Vertigo Nystagmus (horizontal or rotational to the side opposite to the lesion,

more prominent on looking down) Limb ataxia Nausea, vomiting and headache Less common symptoms 40% Diplopia Skew deviation Gaze deviation Facial weakness Dysartria

Gait ataxia 92% Horner sign 88% Dizziness 92%

Moderately common sign 50-70% Dysphagia Hoarseness Vertigo Nystagmus (horizontal or rotational to the side opposite to the lesion,

more prominent on looking down) Limb ataxia Nausea, vomiting and headache Less common symptoms 40% Diplopia Skew deviation Gaze deviation Facial weakness Dysartria

Etiology Pure lateral medullary infarction 67% had VA disease Large artery vessel infarction was the most

frequent cause 15% had dissection 5% cardioembolic Isolated PICA Most likely cardiogenic embolism Less often dissection and VA disease

Etiology Pure lateral medullary infarction 67% had VA disease Large artery vessel infarction was the most

frequent cause 15% had dissection 5% cardioembolic Isolated PICA Most likely cardiogenic embolism Less often dissection and VA disease

57 years old, R Handed gentelman, 7.30 pm, developed sudden onset of profound left sided hemiplegia (arm=leg) associated with left facial drop. He also mentioned dizziness, headache (occipital, non-throbbing, constant) and vomited several times. Denies double vision, visual disturbance. He improved 2 hour later and had left sided weakness and facial drop. However still vomiting and felt dizzy with headache.

57 years old, R Handed gentelman, 7.30 pm, developed sudden onset of profound left sided hemiplegia (arm=leg) associated with left facial drop. He also mentioned dizziness, headache (occipital, non-throbbing, constant) and vomited several times. Denies double vision, visual disturbance. He improved 2 hour later and had left sided weakness and facial drop. However still vomiting and felt dizzy with headache.

PMH of dyslipidemia

NE: Alert, oriented. EOMs were full. Tongue deviated to the right Rotatuar nystagmus on the right gaze. Power on the left upper limb 4/5, Lower limb 4/5 (distal=proximal). Left facial drop, dysartria.

Medial Medullary Syndrome Medial Medullary Syndrome Contralateral arm and leg weakness Ipsilateral weakness of tongue Contralateral loss of position sense Kim et al reported abnormal ocular findings in medial medullary infarction (4/8 ipsilateral to the lesion, 5/8 gaze-evoked) Ocular finding scan be explained by MLF, nucleus prepositus hypglossi or efferent vestibular connection involvement

Neurology 2005;65:1294-1298

Contralateral arm and leg weakness Ipsilateral weakness of tongue Contralateral loss of position sense Kim et al reported abnormal ocular findings in medial medullary infarction (4/8 ipsilateral to the lesion, 5/8 gaze-evoked) Ocular finding scan be explained by MLF, nucleus prepositus hypglossi or efferent vestibular connection involvement

Neurology 2005;65:1294-1298

MainReferences MainReferences J.P Mohr et al. Stroke Pathophysiology, Diagnosis, and Management. Fourth edition. 2005 J Bogousslavsky. Stroke Syndromes. Second Edition. LR Caplan. Caplan`s Stroke. A Clinical Approach. Third Edition G Donnan, B Norrving, J Bamford, J Bogousslavsky. Subcortical stroke. Second edition.

J.P Mohr et al. Stroke Pathophysiology, Diagnosis, and Management. Fourth edition. 2005 J Bogousslavsky. Stroke Syndromes. Second Edition. LR Caplan. Caplan`s Stroke. A Clinical Approach. Third Edition G Donnan, B Norrving, J Bamford, J Bogousslavsky. Subcortical stroke. Second edition.

A 74-year old man with a history of hypertension, diabetes and coronary artery disease developed a sudden onset staggering gait with a tendency to fall to the right. For several hours later he vomited and was confused.

A 74-year old man with a history of hypertension, diabetes and coronary artery disease developed a sudden onset staggering gait with a tendency to fall to the right. For several hours later he vomited and was confused.

Neurological examination showed rotatory nystagmus on left gaze , ataxia on right arm and marked lateropulsion on right when sitting or attemting to stand