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Clinical Program for Cerebrovascular Disorders Mount Sinai Medical Center Cerebellar Infarction Clinical Case Presentation Clara Raquel Epstein, MD Fellow.

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Presentation on theme: "Clinical Program for Cerebrovascular Disorders Mount Sinai Medical Center Cerebellar Infarction Clinical Case Presentation Clara Raquel Epstein, MD Fellow."— Presentation transcript:

1 Clinical Program for Cerebrovascular Disorders Mount Sinai Medical Center Cerebellar Infarction Clinical Case Presentation Clara Raquel Epstein, MD Fellow

2 Cerebellar Infarction Clinical Case Presentation

3 A 69 year old right handed female presented to the Mount Sinai Medical Center Emergency Department after being found on the floor by her brother. One week prior to admission, the patient complained of back pain after moving furniture at home and was placed on Flexaril. On physical exam the vitals were T=39, HR 128, BP 122/98, RR 24. The patient was lethargic, but arrousable and followed simple commands. No other neurologic deficits were appreciated. However coordination and gait testing was deferred secondary to altered mental status.

4 Cerebellar Infarction Hospital Course The patient was transferred to the MICU and an initial evaluation was pursued for possible meningitis vs. sepsis. A head CT without contrast was obtained. On hospital day #2, the patient was re-evaluated and pertinent findings included that the patient was unresponsive with minimally reactive pupils.

5 Cerebellar Infarction Hospital Course Further studies included repeat head CTs, as well as a TEE which revealed a large mobile plaque in the ascending aorta. The patient subsequently underwent an open thoracotomy with clot removal.

6 Diagnostic Studies

7 CT Head 12/29/99

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9 Cerebellar Infarction Discussion

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11 Classification of Cerebellar Dysfunction Developmental –Agenesis –Dandy-Walker Malformation –Arnold Chiri Malformation –Von Hippel Lindau Disease Demyelinative –Multiple Sclerosis –Acute Disseminated Encephalomyelitis

12 Classification of Cerebellar Dysfunction Degenerative –Cerebellar Degeneration –Multi-system Atrophy –Olivopontocerebellar Atrophy Neoplastic –Astrocytoma, Medulloblastoma, Hemangioblastoma, metastasis

13 Classification of Cerebellar Dysfunction Paraneoplastic –Subacute Cerebellar Degeneration Infectious –Abscess Formation –Acute Cerebellitis (viral) –Creutzfeldt-Jacob Disease

14 Classification of Cerebellar Dysfunction Metabolic –Myxoedema –Hypoxia, Hypoglycemia –Alcohol (Vit B1Deficiency) Vascular –Cerebellar Hemorrhage –Cerebellar Infarction Drugs/toxins –Alcohol –Phenytoin

15 Structural Lesions of the Cerebellum Infarcts, Hemorrhages, or tumors – may produce mass effect with enlargement Due to CSF outflow obstruction it can cause: –Hydrocephalus –Increased ICP with papilledema

16 Phylogenetic Subdivisions of the Cerebellum Paleocerebellum (Anterior Lobe) –Receives afferent fibers form the spinal cord (spinocerebellar pathways) –Function: maintenance of gait Neocerebellum (Posterior Lobe) –Receives afferent fibers and projects efferent fibers from and to the motor cortex/vestibular nuclei, basal ganglia and pons –Function: maintenance of postural tone and modulation of motor skills Archicerebellum (Flocculonodular Lobe) –Receives afferent fibers from vestibular system –Function: maintenance of balance

17 Signs and Symptoms of Cerebellar Disorders Ataxia - reeling, wide-based gait Dysmetria - inability to control range of movement Disdiadochokinesia – inability to perform rapid alternating movements Hypotonia – decreased muscle tone

18 Signs and Symptoms of Cerebellar Disorders Decomposition of movement – inability to sequence properly fine, coordinated acts Tremor - intention Dysarthria – with slurring, inappropriate phrasing, and lack of modulation of speech volume (scanning speech) Nystagmus - with the fast component maximal toward the side of the cerebellar lesion

19 Clinical Features Suggestive of Cardiogenic Brain Embolism Primary Features –Abrupt onset of maximal deficit. –Presence of a potential embolic source. –Multiple brain infarcts involving the cortex or cerebellum in multiple vascular territories.

20 Clinical Features Suggestive of Cardiogenic Brain Embolism Secondary Features –Hemorrhagic infarct by CT. –Absence of atherosclerotic vascular disease by angiography –Angiographic evidence of “vanishing occlusions” –Evidence of embolism to other organs. –Cardiac thrombi demonstrated by echo, cardiac CT or MRI.

21 Cardiac Sources of Embolic Stroke

22 Distribution of Associated Infarcts

23 Endocarditis Stroke Risk and Hemorrhage

24 Early Recurrent Embolism after Embolic Stroke

25 Superior Cerebellar Artery Infarction Risk Factors

26 SCA Infarction Symptoms and Signs

27 Anticoagulant Therapy for Embolic Stroke Controversial – Early vs. Delayed Anticoagulant Therapy –Aggregate Data suggests 12% of patients will have a second embolic stroke within 2 weeks. –Immediate heparin reduces the rate of early recurrent embolism Aggregate studies reported a reduction of early recurrent embolism (within 14 days) Risk of symptomatic brain hemorrhage associated with immediate anticoagulation exists Large infarcts appear to be over-represented in hemorrhagic worsening data from the studies reviewed

28 Anticoagulant Therapy for Embolic Stroke Controversial – Early vs. Delayed Anticoagulant Therapy –While iatrogenically exacerbated brain hemorrhage may not be entirely avoidable the following guidelines may be helpful: Immediate anticoagulation of small to moderate-sized embolic strokes may be of overall benefit if a CT hours post stroke shows no hemorrhage Patients with large embolic infarcts –Seem to be at special risk for delayed hemorrhagic transformation –Postponing anticoagulation for 5-7 days may be judicious

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