CEREBELLITIS

 

A.K.A. acute cerebellar ataxia,

Inflammatory process characterized by an acute or subacute onset of cerebellar ataxia following an infection (usually viral; usually GI or respiratory)

 

- Most frequently seen in children 1-6 y.o. and young adults, but may occur in elderly

- 0.05-0.1% of children with varicella infection develop cerebellar ataxia

- In young adults, male:female 2:1 to 4:1

 

Symptoms / Signs

- Ataxia may develop over several hours, days or slowly over a period of 1-4 weeks after infection

- May present as a pure cerebellar syndrome or as part of a more diffuse inflammatory process (brain stem, cerebrum)

 

Cerebellar symptoms/signs

- Dysarthria (45%)

- Ataxia (limb (55%), truncal / gait (42%))

- Oculomotor disturbances (75%)

Impaired smooth pursuit (60%), dysmetria of saccades (55%), impaired suppression of VOR (55%), nystagmus (40%), macro square wave jerks, ocular flutter, opsoclonus (12%)

 

Extracerebellar symptoms/signs

- Cranial nerve palsies

- Uni-/bilateral sensory disturbance

- Hyperreflexia, upgoing plantar responses, increased tone

- Nausea / Vertigo

- Seizures, drowsiness (diffuse inflammation)

 

Etiology of Cerebellitis

***Causative agent not identified in 35% of cases

 

Children

- VZV, Measles, Mumps, EBV, Hepatitis A, Parvovirus B19

- Rubella

- Pertussis

- Q fever (C. burnetti)

- Vaccinations (DTP, MMR, Varicella, Influenza, HepB)

 

Adults

- EBV, influenza, parainfluenza, enterovirus (polio, coxsackie, echo), HSV, VZV, CMV, adenovirus, HIV, mumps

- Lyme (B. burgdorferi)

- Mycoplasma

- Legionella

- Salmonella typhi

- P. falciparum (malaria)

- Rickettsia

 

Differential diagnosis

Infectious

            Listeria

            TB

Demyelinating

            MS, ADEM

Neoplastic

            Cerebellar / Posterior fossa tumor (primary or secondary)

            Neuroblastoma

            Paraneoplastic cerebellar degeneration (PCD)

            Lymphoma

Inflammatory

            Sarcoid

            GBS / Miller Fisher variant (ataxia, ophthalmoplegia, areflexia)

Drugs

            Thallium, lead, barbiturates, dilantin, piperazine, alcohol, solvents, antineoplastic drugs

Hydrocephalus

Foramen magnum compression

 

Investigations

- Serology, acute and convalescent

- Blood films (malaria)

- CSF

            Pleocytosis (WBC up to 250/mcl), 60-99% lymphocytes

            Elevated protein; Glucose normal or slightly reduced

            IgG/albumin ratio: normal in 40%

            Oligoclonal banding: usually absent

            Viral culture / PCR

- EEG / Evoked potentials (Degree of CNS involvement)

- CT / MRI

            Inflammation (bright on T2, gadolinium enhancement)

            Edema / swelling (10-15%)

            Obstructive hydrocephalus

 

Treatment

- IV acyclovir 10mg/kg q8h x 10-14 days

            Reduces duration and severity if given early for VZV or HSV infection

- Lyme disease

            IV ceftriaxone 2g BID x 2 weeks

- Q fever (C. burnetti)

            Minocycline 4mg/kg OD

- Corticosteroids

            Controversial, disease self-limiting

            Depends on severity

            IV methylprednisolone 1g/day x 5 days followed by oral taper

 

Prognosis

- Complete recovery in majority in 1-30 weeks

- Mild to moderate cerebellar deficits in 10% to 40%

- Bad prognostic signs during acute phase: Yawning, hiccoughs, >40 y.o.

- Patients with long term sequelae usually demonstrate moderate to severe cerebellar atrophy

 

References:

The cerebellum and its disorders. Mario Ubaldo Manto and Massimo Pandalfo (ed.), Cambridge University Press, Cambridge UK, 2002, Chapter 16 and references contained therein.

 

Last update: August 2003

Reviewed by: pending review

                                                           

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