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

Stroke localization and syndromes
Objective Stroke definition, symptoms Stroke mimics Stroke syndromes

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).

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.

Case Study
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 .

akinetic mutism contralateral homonymous hemianopsia gaze preference toward the side of the lesion receptive or expressive aphasia (dominant) agnosia (non-dominant) .Major stroke syndromes I Middle cerebral artery (MCA) contralateral hemiparesis contralateral sensory loss arm and face > leg Anterior cerebral artery (ACA) contralateral leg weakness and sensory loss Bilateral: altered mental status. abulia.

Major stroke syndromes II 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 .

diplopia. 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.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. numbness or tingling JAMA 2005. The presence of acute facial paresis. paralysis or weaknes.19:2931-2401 . visual loss.

Misdiagnosis of stroke Norris Lancet 1982.History and physical Further studies – CT head. LP. EEG .1:1523 821 patients consecutively admitted to a stroke unit from ER Evaluators – Interns then neurology Initial studies .

psychogenic. non-convulsive status (5%) Confusional state: metabolic. drugs. alcohol Subdural hematoma CNS tumor Radial-nerve palsy Vertigo Encephalitis Cardiac failure Multiple sclerosis .Misdiagnosis of stroke Norris Lancet 1982.1:1523 Stroke mimic rate 13% Post-ictal state.

Arch Neurol 1995.Conditions that mimic stroke in the ER Libman et al. 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%) .

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

hyponatremia. meningitis Systemic Mass lesions Toxic / Metabolic Migraine with aura (complicated) Hypertensive encephalopathy Multiple sclerosis Transient global amnesia Positional vertigo Psychiatric (‘conversion disorder’) .Mimics of acute ischemic stroke Seizures Vascular lesions Post-ictal “Todd’s paresis” Non-convulsive status epilepticus Intracerebral hemorrhage Extra-axial hemorrhage (EDH. SDH) Subarachnoid hemorrhage Venous sinus thrombosis Tumors or abcess Hypo-/hyper-glycemia. hypercalcemia Drug intoxication Infections Encephalitis.

epilepsy. tongue biting Rapidly improving LOC & deficits Early focal seizures unusual with ischemic stroke Migraine.Clues to non-ischemic etiology Subacute History of trauma. incontinence. malignancy. diabetes Prominent headache Loss of consciousness at onset (ictal) Fluctuating LOC. ICH. mass lesion Positive visual and/or sensory symptoms (“aura”) 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 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 .

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% Useful Questions?? .

ICH 34-44% Stepwise /slutter Thrombosis 32-34%. Embolic 79-82% Thrombotic 40-66%. Lacune 38-54%. Lacune 28-30%.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%. Others <15% Gradual ICH 51-63% .

No headache and neck pain. distal). nausea. vomiting. Upgoing toes on the left. PMH of diabetes and hypertension presented with acute onset left sided facial drop.00 am (Woke up normally). Left facial drop. distal) . oriented. balance problem. Left upper extr power 1/5 (prox. visual disturbance. left lower extr 1/5 (prox. left upper and lower extremity paralysis at 8. duble vision. speech disturbance sensory symptoms. No fluctuations were Observed. Neurological exam: BP 176/89 Alert. She was aware of her deficit.65 years old lady. .

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) .

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. corona radiata . pons. thalamus. internal capsule. Putamen.

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

corona radiata. gait ataxia. 2/3 cases. vertigo is more common in pontine origin PMH . lacunes are in internal capsule Pons (28%). cerebral peduncle and the medullary pyramid Pontine versus internal capsule????? Cannot be distinguished Transient dysartria.PMH ranged from 7-9% in stroke registries.

Pure sensory stroke 6% of LCAS are sensory strokes. anterior limb internal capsule Non-lacunar lesions were found in 0-3% in several studies . 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.

Sensory. corona radiata . internal capsule.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.

Ataxic hemiparesis can be due to internal capsule. . corona radiata. pons . pons involvement. 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.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.

Denied headache. visual disturbance. MRA is completely normal . presented with acute onset of slurred speech and clumsiness on left hand. double vision. vomiting and nausea. left hand impaired alternating movements (slowness of movements). R handed.66 years old gentelman. Neurological exam: Dysartria. vertigo. speech disturbance.

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

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

spreading depression like event. Stereotypic nature of the TIAs preceding lacunar infarction.Capsular warning sign: crescendo subcortical transient ischemic attacks Donnan 1980 described the capsular warning syndrome. pons. Brief bursts of hemiplegia. corona radiata and other adjacent motor pathways Possible mechanisms In situ atheromatous plaque Large vessel atheroma lipping over the penetrator origins Vasospasm Intermittent metabolic dysfunction (Increase in lactate. hemisensory loss or other expressions of LACS and complete resolution between events Basal ganglia. peri-infarct depolarizations) .

putamen. LSAs supply lateral globus pallidus. prognosis and pathogenesis are different . external capsule. the anterior limb of the internal capsule. There are usually 2 medial and 45 lateral LSAs. anterior party of the periventricular corona radiata LSAs are end-arteries and arise with acute angle from main trunk M1 Their presentation.Striocapsular infarcts Defined as large 20 mm> subcortical infarcts in the territory of lentriculostriate arteries. medial putamen. head of caudate.

Repetition was impaired. IV tpa was given at 10. woke up normally and went to bathroom.24 years old gentelman . No gaze palsy. arm and leg. arm and leg. 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.30 his neurological examination revelaed expressive aphasia. Major improvement was seen. Developed sudden onset of right sided paralysis and speech arrest. R handed . He could express himself. Left with right sided hemiparesis (arm>leg)+decreased Pinprick sensation on right side of his body (face. His comprehension was 80% intact. trunk was not involved) . (8.00 am.30 am). visual cut was detected. 9.

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% .

choroidal phelexus of lateral ventricule. posterior twothirds 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. tip of temporal lobe.Anterior choroidal artery infarcts Originates from internal carotid artery First branch of the ICA distal to the posterior communicating artery Supplies optic tract.posterior part of the amygdaloid nucleus. carotid artery atherosclerotic disease . cerebral pedincule. lateral geniculate body.


hemianesthesia. Motor symptoms are due to internal capsule. posterior corona radiata involvement. homonymus hemianopia is rare The most frequent type of presentation is lacunar syndrome 90% cases have motor hemiparesis with or without sensory deficit.AChA territory infarcts represent between 1%10% The classical triad consisting of hemiplegia. 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 According to vascular territories Main trunk occlusion Upper division syndromes Lower division syndromes Branch occlusion According to hemisphere side (Right versus left) .


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

dysprosodia. motor impersistence.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. alexia with agraphia Gerstmann`s syndrome (right-left disorientation. finger agnosia. acalculia and dysgraphia) . constructional apraxia Dominant hemisphere Aphasia. dressing apraxia.

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) .

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

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) 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 Decreased LOC Motor signs Hemiplegia Tetraparesis/tetraplegia Cerebellar Vertigo/dizziness Nausea Sensory abnormalities Headache Ocular abnormalities Bulbar/pseudobulbar 16% 44% 5% 43% 47% 30% 34% 36% 39% 64% .

She leaned to the left when she tried to stand. R handed. had transient attack of dizziness and left face tingling sensation that lasted 15 minutes. Her voice was hoarse.A 57 year-old lady. left ptosis with a smaller pupil. Awakening next day she felt dizzy as if the room were rocking or wavering like a ship. Nystagmus. worse on looking leftward. . She also vomited couple of times and gagged as she tried to swallow water. Decreased palatal motion on the left. NE showed diminished pain and temperature sensation on the left face and right body including limbs.

Lateral Medullary Syndrome .

gait ataxia occurs earlier Dysphagia. sensory Symptoms occur lately . hiccups.Isolated lateral medullary syndrome 75 % occurs suddenly 25% non-sudden Headache. vertigo.

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

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 .

Left facial drop. Power on the left upper limb 4/5. visual disturbance. developed sudden onset of profound left sided hemiplegia (arm=leg) associated with left facial drop.30 pm. headache (occipital. Denies double vision. R Handed gentelman. dysartria.57 years old. non-throbbing. oriented. EOMs were full. He also mentioned dizziness. constant) and vomited several times. PMH of dyslipidemia NE: Alert. Tongue deviated to the right Rotatuar nystagmus on the right gaze. He improved 2 hour later and had left sided weakness and facial drop. . However still vomiting and felt dizzy with headache. 7. Lower limb 4/5 (distal=proximal).


65:1294-1298 . nucleus prepositus hypglossi or efferent vestibular connection involvement Neurology 2005. 5/8 gaze-evoked) Ocular finding scan be explained by MLF.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.

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

diabetes and coronary artery disease developed a sudden onset staggering gait with a tendency to fall to the right. Neurological examination showed rotatory nystagmus on left gaze . ataxia on right arm and marked lateropulsion on right when sitting or attemting to stand . For several hours later he vomited and was confused.A 74-year old man with a history of hypertension.

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