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.<\/p>\n
CASE PRESENTATION<\/strong><\/h2>\nA 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.<\/p>\n
HISTORY & CLINICAL EXAMINATION<\/strong><\/h2>\nThe 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.<\/p>\n
On primary survey, the patient\u2019s 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 SpO\u2082 of 99%. There were no signs of airway obstruction or systemic instability.<\/p>\n
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).<\/p>\n
CNS EXAMINATION<\/strong><\/h2>\nHigher functions: Normal<\/p>\n
Cranial nerves: No facial asymmetry, pupils equal and reactive (2 mm bilaterally)<\/p>\n
Motor system: Power 5\/5 in all four limbs, normal tone, and deep tendon reflexes (DTR) 2+ bilaterally<\/p>\n
Horizontal nystagmus<\/p>\n
Dysarthria+<\/p>\n
Dysmetria with intention tremor (positive finger-nose test and heel-knee test)<\/p>\n
Broad-based ataxic gait<\/p>\n
Positive Romberg\u2019s test (swaying to the left)<\/p>\n
Bilateral plantar reflexes: Flexor response<\/p>\n
INVESTIGATION<\/strong><\/h2>\nLaboratory Results<\/strong><\/p>\nArterial Blood Gas (ABG): Normal pH (7.44), normal PCO\u2082 (39), and bicarbonate (27.1)<\/p>\n
Complete Blood Count (CBC): WBC count of 14,200\/uL (mild leukocytosis)<\/p>\n
Electrolytes: Sodium 133 mEq\/L, potassium 4 mEq\/L, chloride 103 mEq\/L<\/p>\n
Renal Function Tests (RFT) & Liver Function Tests (LFT): Within normal limits<\/p>\n
ECG: Normal sinus rhythm, heart rate 91 bpm, no acute ST-T changes<\/p>\n
Additional Tests Ordered:<\/p>\n
Blood cultures (2 sets)<\/p>\n
Serology tests (for viral and bacterial causes)<\/p>\n
Vitamin B12 levels<\/p>\n
Nerve conduction study<\/p>\n
Based on clinical findings and the absence of structural abnormalities on MRI, a diagnosis of post-infectious cerebellitis was made.<\/p>\n
Treatment and Outcome<\/strong><\/p>\nDay 1 : The patient was started on intravenous methylprednisolone (1 g IV OD for 3 days).<\/p>\n
Day 2 : Improvement in dysarthria was noted.<\/p>\n
Patient was able to walk with one-person support.<\/p>\n
Steroid therapy was continued.<\/p>\n
Day 3 : Patient was shifted to the ward for continued monitoring.<\/p>\n
Day 4 (Discharge Plan)<\/p>\n
The patient showed significant improvement, being able to walk independently with subtle ataxia.<\/p>\n
Discharged with a tapered dose of oral prednisolone (Wysolone) for 15 days.<\/p>\n
Follow-up was advised to assess complete recovery and rehabilitation.<\/p>\n
DISCUSSION<\/strong><\/h2>\nAtaxia 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.<\/p>\n
APPROACH TOWARDS ATAXIA<\/strong><\/h2>\nAtaxia can be classified based on the affected system:<\/p>\n
\n- Cerebellar Ataxia \u2013 Results from dysfunction of the cerebellum or its pathways. It typically presents with dysarthria, intention tremor, nystagmus, and gait disturbances.<\/li>\n
- Sensory Ataxia \u2013 Caused by impaired proprioception due to damage to the dorsal column pathway (e.g., Vitamin B12 deficiency, Tabes dorsalis). Patients have a positive Romberg\u2019s test but lack other cerebellar signs like nystagmus and dysmetria.<\/li>\n
- Vestibular Ataxia \u2013 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).<\/li>\n<\/ol>\n
\n- Romberg\u2019s Test and Sensory Ataxia<\/li>\n<\/ul>\n
Romberg\u2019s test assesses the patient\u2019s ability to maintain balance with their eyes closed.[\/vc_column_text][\/vc_column][\/vc_row][vc_row][vc_column width=”2\/3″][vc_column_text css=”.vc_custom_1741244025517{border-top-width: 2px !important;border-right-width: 2px !important;border-bottom-width: 2px !important;border-left-width: 2px !important;padding-top: 15px !important;padding-right: 15px !important;padding-bottom: 15px !important;padding-left: 15px !important;border-left-color: #0c0c0c !important;border-left-style: solid !important;border-right-color: #0c0c0c !important;border-right-style: solid !important;border-top-color: #0c0c0c !important;border-top-style: solid !important;border-bottom-color: #0c0c0c !important;border-bottom-style: solid !important;}”]To stand upright, individuals require at least two of the following three sensory inputs:<\/p>\n
Proprioception: <\/strong><\/p>\nAwareness of body position in space<\/p>\n
Vestibular Function: <\/strong><\/p>\nAbility to sense head position<\/p>\n
Vision: <\/strong><\/p>\nVisual confirmation of body position<\/p>\n
A positive Romberg\u2019s 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.[\/vc_column_text][\/vc_column][vc_column width=”1\/3″][vc_single_image image=”9828″ img_size=”235×500″][\/vc_column][\/vc_row][vc_row][vc_column][vc_column_text]patient\u2019s ability to maintain balance with their eyes closed.<\/p>\n
\n- Vestibular Ataxia<\/li>\n<\/ul>\n
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\u2019s 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.<\/p>\n
\n- Cerebellar Localization and Its Clinical Features<\/li>\n<\/ul>\n
Different cerebellar regions control specific motor functions:<\/p>\n
![\"\"](\"https:\/\/www.kauveryhospital.com\/ima-journal\/wp-content\/uploads\/2025\/03\/mar-25-img-4.jpg\")
<\/p>\n
Flocculonodular lobe \u2013 Controls eye movements, and dysfunction leads to oculomotor disturbances and nystagmus.<\/p>\n
Paravermis \u2013 Involved in speech coordination, with dysfunction causing dysarthria.<\/p>\n
Vermis \u2013 Regulates axial coordination, and damage results in truncal ataxia and gait instability.<\/p>\n
Lateral Cerebellar Hemispheres \u2013 Control appendicular movements, and lesions result in limb ataxia, dysmetria, and intention tremors.<\/p>\n
Differential Diagnosis of Acute and Subacute Cerebellar Ataxia<\/p>\n
Acute ataxia <\/b><\/strong>(onset within hours to days) can be classified into bilateral and unilateral causes:<\/p>\n\n- Bilateral Causes:<\/li>\n<\/ol>\n
Toxicity: Alcohol, lithium, phenytoin, barbiturates<\/p>\n
Acute viral Cerebellitis<\/p>\n
Post-infectious cerebellitis (e.g., after varicella, Epstein-Barr virus, or mycoplasma infection)<\/p>\n
\n- Unilateral Causes: Vascular events \u2013 Cerebellar infarction or haemorrhage,<\/li>\n<\/ol>\n
Cerebellar abscess<\/p>\n
Subacute ataxia<\/b><\/strong>\u00a0(onset over days to weeks) includes:<\/p>\nBilateral Causes: \u00a0\u00a0Toxicity: Mercury poisoning<\/p>\n
Alcohol-related nutritional deficiencies (Vitamin B1 and B12)<\/p>\n
Chemotherapeutic agents (e.g., ciclosporin, 5-fluorouracil, intrathecal methotrexate, procarbazine)<\/p>\n
Unilateral Causes:Neoplastic conditions , Demyelinating diseases such as multiple sclerosis<\/p>\n
POST INFECTIOUS CERBELLITIS<\/strong><\/h2>\nCerebellitis 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.<\/p>\n
![\"\"](\"https:\/\/www.kauveryhospital.com\/ima-journal\/wp-content\/uploads\/2025\/03\/mar-25-img-5.jpg\")
[\/vc_column_text][\/vc_column][\/vc_row][vc_row][vc_column width=”1\/2″][vc_column_text css=”.vc_custom_1741244081023{border-top-width: 2px !important;border-right-width: 2px !important;border-bottom-width: 2px !important;border-left-width: 2px !important;padding-top: 10px !important;padding-right: 10px !important;padding-bottom: 10px !important;padding-left: 10px !important;border-left-color: #0c0c0c !important;border-left-style: solid !important;border-right-color: #0c0c0c !important;border-right-style: solid !important;border-top-color: #0c0c0c !important;border-top-style: solid !important;border-bottom-color: #0c0c0c !important;border-bottom-style: solid !important;}”]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.[\/vc_column_text][\/vc_column][vc_column width=”1\/2″][vc_column_text css=”.vc_custom_1741244068140{border-top-width: 2px !important;border-right-width: 2px !important;border-bottom-width: 2px !important;border-left-width: 2px !important;padding-top: 10px !important;padding-right: 10px !important;padding-bottom: 10px !important;padding-left: 10px !important;border-left-color: #0c0c0c !important;border-left-style: solid !important;border-right-color: #0c0c0c !important;border-right-style: solid !important;border-top-color: #0c0c0c !important;border-top-style: solid !important;border-bottom-color: #0c0c0c !important;border-bottom-style: solid !important;}”]HMPAO-SPECT – technetium-99m hexamethyl propylene amine Oxime single-photon emission computed tomography;<\/p>\n
H-MRS Proton magnetic resonance spectroscopy;<\/p>\n
PET – position emission<\/p>\n
Tomography[\/vc_column_text][\/vc_column][\/vc_row][vc_row][vc_column][vc_column_text]<\/p>\n
CONCLUSION<\/strong><\/h2>\nA 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.<\/p>\n
REFERENCES<\/strong><\/h2>\nHandbook of clinical neurology (ataxic disorders) Acquired ataxias, infectious and para-infectious<\/p>\n
Acute cerebellar ataxia after Epstein-Barr -Virus infection<\/p>\n
Stephanie L. Barnes, MBBS (Hons), BSc (Adv), and Bruce J. Brew, MBBS, MD, DSc<\/p>\n
Neurology: Clinical Practice 00 2019 vol. 0 no. 0 1-2 doi:10.1212\/CPJ.0000000000000659<\/p>\n
Acute cerebellitis in adults: a case report<\/p>\n
And review of the literature Van Samkar1*, M. N. F. Poulsen2, H. P. Bienfait3 And R. B. Van Leeuwen3<\/p>\n
![\"\"](\"https:\/\/www.kauveryhospital.com\/ima-journal\/wp-content\/uploads\/2024\/12\/dr.avinas-150x150.jpg\")
Dr. Avinash. S<\/strong>
\nEmergency Medicine Resident,<\/em>
\nDepartment of Emergency Medicine,<\/em>
\nKauvery Hospital- Alwarpet<\/p>\n <\/p>\n
<\/p>\n
![\"\"](\"https:\/\/www.kauveryhospital.com\/ima-journal\/wp-content\/uploads\/2024\/10\/Dr_Ashok-150x150.jpg\")
Dr. Ashok Nandagopal<\/strong>
\nClinical Lead & Consultant,<\/em>
\nDepartment of Emergency Medicine,<\/em>
\nKauvery Hospital- Alwarpet[\/vc_column_text][\/vc_column][\/vc_row]<\/p>\n","protected":false},"excerpt":{"rendered":"[vc_row][vc_column][vc_column_text] 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<\/p>\n","protected":false},"author":2,"featured_media":9825,"comment_status":"closed","ping_status":"open","sticky":false,"template":"","format":"standard","meta":{"footnotes":""},"categories":[86],"tags":[],"class_list":["post-9824","post","type-post","status-publish","format-standard","has-post-thumbnail","hentry","category-ima-journal-march-2025"],"yoast_head":"\n
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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.<\/p>\n
On primary survey, the patient\u2019s 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 SpO\u2082 of 99%. There were no signs of airway obstruction or systemic instability.<\/p>\n
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).<\/p>\n
CNS EXAMINATION<\/strong><\/h2>\nHigher functions: Normal<\/p>\n
Cranial nerves: No facial asymmetry, pupils equal and reactive (2 mm bilaterally)<\/p>\n
Motor system: Power 5\/5 in all four limbs, normal tone, and deep tendon reflexes (DTR) 2+ bilaterally<\/p>\n
Horizontal nystagmus<\/p>\n
Dysarthria+<\/p>\n
Dysmetria with intention tremor (positive finger-nose test and heel-knee test)<\/p>\n
Broad-based ataxic gait<\/p>\n
Positive Romberg\u2019s test (swaying to the left)<\/p>\n
Bilateral plantar reflexes: Flexor response<\/p>\n
INVESTIGATION<\/strong><\/h2>\nLaboratory Results<\/strong><\/p>\nArterial Blood Gas (ABG): Normal pH (7.44), normal PCO\u2082 (39), and bicarbonate (27.1)<\/p>\n
Complete Blood Count (CBC): WBC count of 14,200\/uL (mild leukocytosis)<\/p>\n
Electrolytes: Sodium 133 mEq\/L, potassium 4 mEq\/L, chloride 103 mEq\/L<\/p>\n
Renal Function Tests (RFT) & Liver Function Tests (LFT): Within normal limits<\/p>\n
ECG: Normal sinus rhythm, heart rate 91 bpm, no acute ST-T changes<\/p>\n
Additional Tests Ordered:<\/p>\n
Blood cultures (2 sets)<\/p>\n
Serology tests (for viral and bacterial causes)<\/p>\n
Vitamin B12 levels<\/p>\n
Nerve conduction study<\/p>\n
Based on clinical findings and the absence of structural abnormalities on MRI, a diagnosis of post-infectious cerebellitis was made.<\/p>\n
Treatment and Outcome<\/strong><\/p>\nDay 1 : The patient was started on intravenous methylprednisolone (1 g IV OD for 3 days).<\/p>\n
Day 2 : Improvement in dysarthria was noted.<\/p>\n
Patient was able to walk with one-person support.<\/p>\n
Steroid therapy was continued.<\/p>\n
Day 3 : Patient was shifted to the ward for continued monitoring.<\/p>\n
Day 4 (Discharge Plan)<\/p>\n
The patient showed significant improvement, being able to walk independently with subtle ataxia.<\/p>\n
Discharged with a tapered dose of oral prednisolone (Wysolone) for 15 days.<\/p>\n
Follow-up was advised to assess complete recovery and rehabilitation.<\/p>\n
DISCUSSION<\/strong><\/h2>\nAtaxia 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.<\/p>\n
APPROACH TOWARDS ATAXIA<\/strong><\/h2>\nAtaxia can be classified based on the affected system:<\/p>\n
\n- Cerebellar Ataxia \u2013 Results from dysfunction of the cerebellum or its pathways. It typically presents with dysarthria, intention tremor, nystagmus, and gait disturbances.<\/li>\n
- Sensory Ataxia \u2013 Caused by impaired proprioception due to damage to the dorsal column pathway (e.g., Vitamin B12 deficiency, Tabes dorsalis). Patients have a positive Romberg\u2019s test but lack other cerebellar signs like nystagmus and dysmetria.<\/li>\n
- Vestibular Ataxia \u2013 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).<\/li>\n<\/ol>\n
\n- Romberg\u2019s Test and Sensory Ataxia<\/li>\n<\/ul>\n
Romberg\u2019s test assesses the patient\u2019s ability to maintain balance with their eyes closed.[\/vc_column_text][\/vc_column][\/vc_row][vc_row][vc_column width=”2\/3″][vc_column_text css=”.vc_custom_1741244025517{border-top-width: 2px !important;border-right-width: 2px !important;border-bottom-width: 2px !important;border-left-width: 2px !important;padding-top: 15px !important;padding-right: 15px !important;padding-bottom: 15px !important;padding-left: 15px !important;border-left-color: #0c0c0c !important;border-left-style: solid !important;border-right-color: #0c0c0c !important;border-right-style: solid !important;border-top-color: #0c0c0c !important;border-top-style: solid !important;border-bottom-color: #0c0c0c !important;border-bottom-style: solid !important;}”]To stand upright, individuals require at least two of the following three sensory inputs:<\/p>\n
Proprioception: <\/strong><\/p>\nAwareness of body position in space<\/p>\n
Vestibular Function: <\/strong><\/p>\nAbility to sense head position<\/p>\n
Vision: <\/strong><\/p>\nVisual confirmation of body position<\/p>\n
A positive Romberg\u2019s 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.[\/vc_column_text][\/vc_column][vc_column width=”1\/3″][vc_single_image image=”9828″ img_size=”235×500″][\/vc_column][\/vc_row][vc_row][vc_column][vc_column_text]patient\u2019s ability to maintain balance with their eyes closed.<\/p>\n
\n- Vestibular Ataxia<\/li>\n<\/ul>\n
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\u2019s 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.<\/p>\n
\n- Cerebellar Localization and Its Clinical Features<\/li>\n<\/ul>\n
Different cerebellar regions control specific motor functions:<\/p>\n
<\/p>\n
Flocculonodular lobe \u2013 Controls eye movements, and dysfunction leads to oculomotor disturbances and nystagmus.<\/p>\n
Paravermis \u2013 Involved in speech coordination, with dysfunction causing dysarthria.<\/p>\n
Vermis \u2013 Regulates axial coordination, and damage results in truncal ataxia and gait instability.<\/p>\n
Lateral Cerebellar Hemispheres \u2013 Control appendicular movements, and lesions result in limb ataxia, dysmetria, and intention tremors.<\/p>\n
Differential Diagnosis of Acute and Subacute Cerebellar Ataxia<\/p>\n
Acute ataxia <\/b><\/strong>(onset within hours to days) can be classified into bilateral and unilateral causes:<\/p>\n\n- Bilateral Causes:<\/li>\n<\/ol>\n
Toxicity: Alcohol, lithium, phenytoin, barbiturates<\/p>\n
Acute viral Cerebellitis<\/p>\n
Post-infectious cerebellitis (e.g., after varicella, Epstein-Barr virus, or mycoplasma infection)<\/p>\n
\n- Unilateral Causes: Vascular events \u2013 Cerebellar infarction or haemorrhage,<\/li>\n<\/ol>\n
Cerebellar abscess<\/p>\n
Subacute ataxia<\/b><\/strong>\u00a0(onset over days to weeks) includes:<\/p>\nBilateral Causes: \u00a0\u00a0Toxicity: Mercury poisoning<\/p>\n
Alcohol-related nutritional deficiencies (Vitamin B1 and B12)<\/p>\n
Chemotherapeutic agents (e.g., ciclosporin, 5-fluorouracil, intrathecal methotrexate, procarbazine)<\/p>\n
Unilateral Causes:Neoplastic conditions , Demyelinating diseases such as multiple sclerosis<\/p>\n
POST INFECTIOUS CERBELLITIS<\/strong><\/h2>\nCerebellitis 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.<\/p>\n
[\/vc_column_text][\/vc_column][\/vc_row][vc_row][vc_column width=”1\/2″][vc_column_text css=”.vc_custom_1741244081023{border-top-width: 2px !important;border-right-width: 2px !important;border-bottom-width: 2px !important;border-left-width: 2px !important;padding-top: 10px !important;padding-right: 10px !important;padding-bottom: 10px !important;padding-left: 10px !important;border-left-color: #0c0c0c !important;border-left-style: solid !important;border-right-color: #0c0c0c !important;border-right-style: solid !important;border-top-color: #0c0c0c !important;border-top-style: solid !important;border-bottom-color: #0c0c0c !important;border-bottom-style: solid !important;}”]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.[\/vc_column_text][\/vc_column][vc_column width=”1\/2″][vc_column_text css=”.vc_custom_1741244068140{border-top-width: 2px !important;border-right-width: 2px !important;border-bottom-width: 2px !important;border-left-width: 2px !important;padding-top: 10px !important;padding-right: 10px !important;padding-bottom: 10px !important;padding-left: 10px !important;border-left-color: #0c0c0c !important;border-left-style: solid !important;border-right-color: #0c0c0c !important;border-right-style: solid !important;border-top-color: #0c0c0c !important;border-top-style: solid !important;border-bottom-color: #0c0c0c !important;border-bottom-style: solid !important;}”]HMPAO-SPECT – technetium-99m hexamethyl propylene amine Oxime single-photon emission computed tomography;<\/p>\n
H-MRS Proton magnetic resonance spectroscopy;<\/p>\n
PET – position emission<\/p>\n
Tomography[\/vc_column_text][\/vc_column][\/vc_row][vc_row][vc_column][vc_column_text]<\/p>\n
CONCLUSION<\/strong><\/h2>\nA 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.<\/p>\n
REFERENCES<\/strong><\/h2>\nHandbook of clinical neurology (ataxic disorders) Acquired ataxias, infectious and para-infectious<\/p>\n
Acute cerebellar ataxia after Epstein-Barr -Virus infection<\/p>\n
Stephanie L. Barnes, MBBS (Hons), BSc (Adv), and Bruce J. Brew, MBBS, MD, DSc<\/p>\n
Neurology: Clinical Practice 00 2019 vol. 0 no. 0 1-2 doi:10.1212\/CPJ.0000000000000659<\/p>\n
Acute cerebellitis in adults: a case report<\/p>\n
And review of the literature Van Samkar1*, M. N. F. Poulsen2, H. P. Bienfait3 And R. B. Van Leeuwen3<\/p>\n
Dr. Avinash. S<\/strong>
\nEmergency Medicine Resident,<\/em>
\nDepartment of Emergency Medicine,<\/em>
\nKauvery Hospital- Alwarpet<\/p>\n <\/p>\n
<\/p>\n
Dr. Ashok Nandagopal<\/strong>
\nClinical Lead & Consultant,<\/em>
\nDepartment of Emergency Medicine,<\/em>
\nKauvery Hospital- Alwarpet[\/vc_column_text][\/vc_column][\/vc_row]<\/p>\n","protected":false},"excerpt":{"rendered":"[vc_row][vc_column][vc_column_text] 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<\/p>\n","protected":false},"author":2,"featured_media":9825,"comment_status":"closed","ping_status":"open","sticky":false,"template":"","format":"standard","meta":{"footnotes":""},"categories":[86],"tags":[],"class_list":["post-9824","post","type-post","status-publish","format-standard","has-post-thumbnail","hentry","category-ima-journal-march-2025"],"yoast_head":"\n
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Laboratory Results<\/strong><\/p>\n Arterial Blood Gas (ABG): Normal pH (7.44), normal PCO\u2082 (39), and bicarbonate (27.1)<\/p>\n Complete Blood Count (CBC): WBC count of 14,200\/uL (mild leukocytosis)<\/p>\n Electrolytes: Sodium 133 mEq\/L, potassium 4 mEq\/L, chloride 103 mEq\/L<\/p>\n Renal Function Tests (RFT) & Liver Function Tests (LFT): Within normal limits<\/p>\n ECG: Normal sinus rhythm, heart rate 91 bpm, no acute ST-T changes<\/p>\n Additional Tests Ordered:<\/p>\n Blood cultures (2 sets)<\/p>\n Serology tests (for viral and bacterial causes)<\/p>\n Vitamin B12 levels<\/p>\n Nerve conduction study<\/p>\n Based on clinical findings and the absence of structural abnormalities on MRI, a diagnosis of post-infectious cerebellitis was made.<\/p>\n Treatment and Outcome<\/strong><\/p>\n Day 1 : The patient was started on intravenous methylprednisolone (1 g IV OD for 3 days).<\/p>\n Day 2 : Improvement in dysarthria was noted.<\/p>\n Patient was able to walk with one-person support.<\/p>\n Steroid therapy was continued.<\/p>\n Day 3 : Patient was shifted to the ward for continued monitoring.<\/p>\n Day 4 (Discharge Plan)<\/p>\n The patient showed significant improvement, being able to walk independently with subtle ataxia.<\/p>\n Discharged with a tapered dose of oral prednisolone (Wysolone) for 15 days.<\/p>\n Follow-up was advised to assess complete recovery and rehabilitation.<\/p>\n 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.<\/p>\n Ataxia can be classified based on the affected system:<\/p>\n Romberg\u2019s test assesses the patient\u2019s ability to maintain balance with their eyes closed.[\/vc_column_text][\/vc_column][\/vc_row][vc_row][vc_column width=”2\/3″][vc_column_text css=”.vc_custom_1741244025517{border-top-width: 2px !important;border-right-width: 2px !important;border-bottom-width: 2px !important;border-left-width: 2px !important;padding-top: 15px !important;padding-right: 15px !important;padding-bottom: 15px !important;padding-left: 15px !important;border-left-color: #0c0c0c !important;border-left-style: solid !important;border-right-color: #0c0c0c !important;border-right-style: solid !important;border-top-color: #0c0c0c !important;border-top-style: solid !important;border-bottom-color: #0c0c0c !important;border-bottom-style: solid !important;}”]To stand upright, individuals require at least two of the following three sensory inputs:<\/p>\n Proprioception: <\/strong><\/p>\n Awareness of body position in space<\/p>\n Vestibular Function: <\/strong><\/p>\n Ability to sense head position<\/p>\n Vision: <\/strong><\/p>\n Visual confirmation of body position<\/p>\n A positive Romberg\u2019s 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.[\/vc_column_text][\/vc_column][vc_column width=”1\/3″][vc_single_image image=”9828″ img_size=”235×500″][\/vc_column][\/vc_row][vc_row][vc_column][vc_column_text]patient\u2019s ability to maintain balance with their eyes closed.<\/p>\n 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\u2019s 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.<\/p>\n Different cerebellar regions control specific motor functions:<\/p>\n Flocculonodular lobe \u2013 Controls eye movements, and dysfunction leads to oculomotor disturbances and nystagmus.<\/p>\n Paravermis \u2013 Involved in speech coordination, with dysfunction causing dysarthria.<\/p>\n Vermis \u2013 Regulates axial coordination, and damage results in truncal ataxia and gait instability.<\/p>\n Lateral Cerebellar Hemispheres \u2013 Control appendicular movements, and lesions result in limb ataxia, dysmetria, and intention tremors.<\/p>\n Differential Diagnosis of Acute and Subacute Cerebellar Ataxia<\/p>\n Acute ataxia <\/b><\/strong>(onset within hours to days) can be classified into bilateral and unilateral causes:<\/p>\n Toxicity: Alcohol, lithium, phenytoin, barbiturates<\/p>\n Acute viral Cerebellitis<\/p>\n Post-infectious cerebellitis (e.g., after varicella, Epstein-Barr virus, or mycoplasma infection)<\/p>\n Cerebellar abscess<\/p>\n Subacute ataxia<\/b><\/strong>\u00a0(onset over days to weeks) includes:<\/p>\n Bilateral Causes: \u00a0\u00a0Toxicity: Mercury poisoning<\/p>\n Alcohol-related nutritional deficiencies (Vitamin B1 and B12)<\/p>\n Chemotherapeutic agents (e.g., ciclosporin, 5-fluorouracil, intrathecal methotrexate, procarbazine)<\/p>\n Unilateral Causes:Neoplastic conditions , Demyelinating diseases such as multiple sclerosis<\/p>\n 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.<\/p>\n H-MRS Proton magnetic resonance spectroscopy;<\/p>\n PET – position emission<\/p>\n Tomography[\/vc_column_text][\/vc_column][\/vc_row][vc_row][vc_column][vc_column_text]<\/p>\n 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.<\/p>\n Handbook of clinical neurology (ataxic disorders) Acquired ataxias, infectious and para-infectious<\/p>\n Acute cerebellar ataxia after Epstein-Barr -Virus infection<\/p>\n Stephanie L. Barnes, MBBS (Hons), BSc (Adv), and Bruce J. Brew, MBBS, MD, DSc<\/p>\n Neurology: Clinical Practice 00 2019 vol. 0 no. 0 1-2 doi:10.1212\/CPJ.0000000000000659<\/p>\n Acute cerebellitis in adults: a case report<\/p>\n And review of the literature Van Samkar1*, M. N. F. Poulsen2, H. P. Bienfait3 And R. B. Van Leeuwen3<\/p>\n <\/p>\n <\/p>\n [vc_row][vc_column][vc_column_text] 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<\/p>\n","protected":false},"author":2,"featured_media":9825,"comment_status":"closed","ping_status":"open","sticky":false,"template":"","format":"standard","meta":{"footnotes":""},"categories":[86],"tags":[],"class_list":["post-9824","post","type-post","status-publish","format-standard","has-post-thumbnail","hentry","category-ima-journal-march-2025"],"yoast_head":"\nDISCUSSION<\/strong><\/h2>\n
APPROACH TOWARDS ATAXIA<\/strong><\/h2>\n
\n
\n
\n
\n
<\/p>\n\n
\n
POST INFECTIOUS CERBELLITIS<\/strong><\/h2>\n
[\/vc_column_text][\/vc_column][\/vc_row][vc_row][vc_column width=”1\/2″][vc_column_text css=”.vc_custom_1741244081023{border-top-width: 2px !important;border-right-width: 2px !important;border-bottom-width: 2px !important;border-left-width: 2px !important;padding-top: 10px !important;padding-right: 10px !important;padding-bottom: 10px !important;padding-left: 10px !important;border-left-color: #0c0c0c !important;border-left-style: solid !important;border-right-color: #0c0c0c !important;border-right-style: solid !important;border-top-color: #0c0c0c !important;border-top-style: solid !important;border-bottom-color: #0c0c0c !important;border-bottom-style: solid !important;}”]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.[\/vc_column_text][\/vc_column][vc_column width=”1\/2″][vc_column_text css=”.vc_custom_1741244068140{border-top-width: 2px !important;border-right-width: 2px !important;border-bottom-width: 2px !important;border-left-width: 2px !important;padding-top: 10px !important;padding-right: 10px !important;padding-bottom: 10px !important;padding-left: 10px !important;border-left-color: #0c0c0c !important;border-left-style: solid !important;border-right-color: #0c0c0c !important;border-right-style: solid !important;border-top-color: #0c0c0c !important;border-top-style: solid !important;border-bottom-color: #0c0c0c !important;border-bottom-style: solid !important;}”]HMPAO-SPECT – technetium-99m hexamethyl propylene amine Oxime single-photon emission computed tomography;<\/p>\nCONCLUSION<\/strong><\/h2>\n
REFERENCES<\/strong><\/h2>\n
Dr. Avinash. S<\/strong>
\nEmergency Medicine Resident,<\/em>
\nDepartment of Emergency Medicine,<\/em>
\nKauvery Hospital- Alwarpet<\/p>\nDr. Ashok Nandagopal<\/strong>
\nClinical Lead & Consultant,<\/em>
\nDepartment of Emergency Medicine,<\/em>
\nKauvery Hospital- Alwarpet[\/vc_column_text][\/vc_column][\/vc_row]<\/p>\n","protected":false},"excerpt":{"rendered":"