Post-Infectious Cerebellitis: A Case Report and Management Approach

Post-Infectious Cerebellitis: A Case Report and Management Approach
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INTRODUCTION

Post-infectious cerebellitis is an inflammatory condition of the cerebellum, often occurring after a viral or bacterial infection. It presents with ataxia, dysarthria, nystagmus, and other cerebellar dysfunctions. While the condition is usually self-limiting, early diagnosis and appropriate management are crucial for better patient outcomes. This article presents a case of post-infectious cerebellitis in a 42-year-old male, detailing his presentation, diagnostic approach, and treatment course.

CASE PRESENTATION

A 42-year-old gentleman was transferred to our emergency department (ER) from an outside hospital with complaints of slurred speech, loss of balance, and difficulty in standing and walking for the past two days. He was initially evaluated at another hospital, where an MRI brain on day 1 and an MRI brain with whole spine contrast on day 2 were reported as normal. Due to persistent symptoms, he was referred for further management.

HISTORY & CLINICAL EXAMINATION

The patient had a history of fever with cough and yellow-colored expectoration 10 days prior, which was treated at a local clinic with intravenous antibiotics for three days. The fever and respiratory symptoms had resolved three days before his current symptoms appeared.

On primary survey, the patient’s vital signs were stable, with a Glasgow Coma Scale (GCS) of 15/15, a heart rate of 104 bpm, respiratory rate of 26 bpm, blood pressure of 130/80 mmHg, and SpO₂ of 99%. There were no signs of airway obstruction or systemic instability.

A secondary survey revealed no known drug allergies (NKDA), no past medical or surgical history, and no recent intake of neurotoxic substances. His medications from the previous hospital stay included Inj piperacillin-tazobactam (4.5 g TDS), Inj doxycycline (100 mg BD), Tab aspirin (150 mg OD), and Tab atorvastatin (20 mg HS).

CNS EXAMINATION

Higher functions: Normal

Cranial nerves: No facial asymmetry, pupils equal and reactive (2 mm bilaterally)

Motor system: Power 5/5 in all four limbs, normal tone, and deep tendon reflexes (DTR) 2+ bilaterally

Horizontal nystagmus

Dysarthria+

Dysmetria with intention tremor (positive finger-nose test and heel-knee test)

Broad-based ataxic gait

Positive Romberg’s test (swaying to the left)

Bilateral plantar reflexes: Flexor response

INVESTIGATION

Laboratory Results

Arterial Blood Gas (ABG): Normal pH (7.44), normal PCO₂ (39), and bicarbonate (27.1)

Complete Blood Count (CBC): WBC count of 14,200/uL (mild leukocytosis)

Electrolytes: Sodium 133 mEq/L, potassium 4 mEq/L, chloride 103 mEq/L

Renal Function Tests (RFT) & Liver Function Tests (LFT): Within normal limits

ECG: Normal sinus rhythm, heart rate 91 bpm, no acute ST-T changes

Additional Tests Ordered:

Blood cultures (2 sets)

Serology tests (for viral and bacterial causes)

Vitamin B12 levels

Nerve conduction study

Based on clinical findings and the absence of structural abnormalities on MRI, a diagnosis of post-infectious cerebellitis was made.

Treatment and Outcome

Day 1 : The patient was started on intravenous methylprednisolone (1 g IV OD for 3 days).

Day 2 : Improvement in dysarthria was noted.

Patient was able to walk with one-person support.

Steroid therapy was continued.

Day 3 : Patient was shifted to the ward for continued monitoring.

Day 4 (Discharge Plan)

The patient showed significant improvement, being able to walk independently with subtle ataxia.

Discharged with a tapered dose of oral prednisolone (Wysolone) for 15 days.

Follow-up was advised to assess complete recovery and rehabilitation.

DISCUSSION

Ataxia is a neurological condition characterized by impaired coordination, which can result from dysfunction in the cerebellum and its connections, the proprioceptive sensory pathway, or the vestibular system. Understanding the underlying pathophysiology and differentiating between these types of ataxia is essential for accurate diagnosis and effective management.

APPROACH TOWARDS ATAXIA

Ataxia can be classified based on the affected system:

  1. Cerebellar Ataxia – Results from dysfunction of the cerebellum or its pathways. It typically presents with dysarthria, intention tremor, nystagmus, and gait disturbances.
  2. Sensory Ataxia – Caused by impaired proprioception due to damage to the dorsal column pathway (e.g., Vitamin B12 deficiency, Tabes dorsalis). Patients have a positive Romberg’s test but lack other cerebellar signs like nystagmus and dysmetria.
  3. Vestibular Ataxia – Arises from peripheral or central vestibular dysfunction. It presents with vertigo, nystagmus, abnormal head impulse test, and sometimes hearing disturbances (e.g., vestibular neuritis, aminoglycoside toxicity).
  • Romberg’s Test and Sensory Ataxia

Romberg’s test assesses the patient’s ability to maintain balance with their eyes closed.

To stand upright, individuals require at least two of the following three sensory inputs:

Proprioception:

Awareness of body position in space

Vestibular Function:

Ability to sense head position

Vision:

Visual confirmation of body position

A positive Romberg’s test suggests a proprioceptive deficit rather than a cerebellar disorder. Sensory ataxia due to Vitamin B12 deficiency or Tabes dorsalis leads to imbalance that worsens with eyes closed, without associated cerebellar signs like dysmetria or nystagmus.

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patient’s ability to maintain balance with their eyes closed.

  • Vestibular Ataxia

Vestibular dysfunction can lead to ataxia without cerebellar involvement. Peripheral vestibular disorders, such as vestibular neuritis or drug-induced vestibulopathy (aminoglycosides), can impair balance. Patients may exhibit nystagmus, positive Romberg’s test, past pointing, and abnormal head impulse test, often accompanied by vertigo, nausea, vomiting, and hearing disturbances. Unlike cerebellar ataxia, dysarthria is not a feature of vestibular ataxia.

  • Cerebellar Localization and Its Clinical Features

Different cerebellar regions control specific motor functions:

Flocculonodular lobe – Controls eye movements, and dysfunction leads to oculomotor disturbances and nystagmus.

Paravermis – Involved in speech coordination, with dysfunction causing dysarthria.

Vermis – Regulates axial coordination, and damage results in truncal ataxia and gait instability.

Lateral Cerebellar Hemispheres – Control appendicular movements, and lesions result in limb ataxia, dysmetria, and intention tremors.

Differential Diagnosis of Acute and Subacute Cerebellar Ataxia

Acute ataxia (onset within hours to days) can be classified into bilateral and unilateral causes:

  1. Bilateral Causes:

Toxicity: Alcohol, lithium, phenytoin, barbiturates

Acute viral Cerebellitis

Post-infectious cerebellitis (e.g., after varicella, Epstein-Barr virus, or mycoplasma infection)

  1. Unilateral Causes: Vascular events – Cerebellar infarction or haemorrhage,

Cerebellar abscess

Subacute ataxia (onset over days to weeks) includes:

Bilateral Causes:   Toxicity: Mercury poisoning

Alcohol-related nutritional deficiencies (Vitamin B1 and B12)

Chemotherapeutic agents (e.g., ciclosporin, 5-fluorouracil, intrathecal methotrexate, procarbazine)

Unilateral Causes:Neoplastic conditions , Demyelinating diseases such as multiple sclerosis

POST INFECTIOUS CERBELLITIS

Cerebellitis is considered an inflammatory disorder of the cerebellum that can affect both children and adults. It may be linked to infections, either directly or indirectly. When ataxia develops during the course of an illness, it is typically classified as infectious. If there is a gap of several weeks between the initial infection and the onset of ataxia, it is referred to as para-infectious or post-infectious. In cases where ataxia emerges within a few days of vaccination, it is described as post-vaccinal in origin.

Once cerebellitis is clinically diagnosed and other conditions have been excluded, management should follow a structured approach. Neuroimaging plays a crucial role in detecting rare cases with cerebellar edema and secondary hydrocephalus. A lumbar puncture can aid in identifying infectious causes, though a lack of pleocytosis does not rule out a para-infectious autoimmune process.

HMPAO-SPECT – technetium-99m hexamethyl propylene amine Oxime single-photon emission computed tomography;

H-MRS Proton magnetic resonance spectroscopy;

PET – position emission

Tomography

CONCLUSION

A structured approach to evaluating ataxia is crucial for identifying the underlying pathology. In our case, the acute onset of symptoms following a recent infection, along with normal imaging and cerebellar signs, strongly supported post-infectious cerebellitis. Early recognition and treatment with corticosteroids led to significant improvement, highlighting the importance of prompt intervention in immune-mediated ataxias.

REFERENCES

Handbook of clinical neurology (ataxic disorders) Acquired ataxias, infectious and para-infectious

Acute cerebellar ataxia after Epstein-Barr -Virus infection

Stephanie L. Barnes, MBBS (Hons), BSc (Adv), and Bruce J. Brew, MBBS, MD, DSc

Neurology: Clinical Practice 00 2019 vol. 0 no. 0 1-2 doi:10.1212/CPJ.0000000000000659

Acute cerebellitis in adults: a case report

And review of the literature Van Samkar1*, M. N. F. Poulsen2, H. P. Bienfait3 And R. B. Van Leeuwen3

Dr. Avinash. S
Emergency Medicine Resident,
Department of Emergency Medicine,
Kauvery Hospital- Alwarpet

 

 

Dr. Ashok Nandagopal
Clinical Lead & Consultant,
Department of Emergency Medicine,
Kauvery Hospital- Alwarpet