Clinical Program for Cerebrovascular Disorders Mount Sinai Medical

							  Clinical Program for
Cerebrovascular Disorders
 Mount Sinai Medical Center




    Cerebellar Infarction
  Clinical Case Presentation
 Clara Raquel Epstein, MD Fellow
Cerebellar Infarction
    Clinical Case Presentation
        Cerebellar Infarction
        Clinical Case Presentation
• 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.
        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.
        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.
Diagnostic Studies
CT Head 12/29/99
CT Head 12/29/99
Cerebellar Infarction
    Discussion
      Classification of Cerebellar
              Dysfunction
• Developmental
  –   Agenesis
  –   Dandy-Walker Malformation
  –   Arnold Chiri Malformation
  –   Von Hippel Lindau Disease
• Demyelinative
  – Multiple Sclerosis
  – Acute Disseminated Encephalomyelitis
    Classification of Cerebellar
            Dysfunction
• Degenerative
  – Cerebellar Degeneration
  – Multi-system Atrophy
  – Olivopontocerebellar Atrophy
• Neoplastic
  – Astrocytoma, Medulloblastoma,
    Hemangioblastoma, metastasis
    Classification of Cerebellar
            Dysfunction
• Paraneoplastic
  – Subacute Cerebellar Degeneration
• Infectious
  – Abscess Formation
  – Acute Cerebellitis (viral)
  – Creutzfeldt-Jacob Disease
    Classification of Cerebellar
            Dysfunction
• Metabolic
  – Myxoedema
  – Hypoxia, Hypoglycemia
  – Alcohol (Vit B1Deficiency)
• Vascular
  – Cerebellar Hemorrhage
  – Cerebellar Infarction
• Drugs/toxins
  – Alcohol
  – Phenytoin
      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
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
      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
        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
 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.
 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.
Cardiac Sources of Embolic
          Stroke
Distribution of Associated
          Infarcts
Endocarditis Stroke Risk and
       Hemorrhage
Early Recurrent Embolism after
       Embolic Stroke
Superior Cerebellar Artery
 Infarction Risk Factors
  SCA Infarction
Symptoms and Signs
     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
     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 24-48 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