Praveen Kesav

Teaching NeuroImages: Deep gray matter involvement in neurobrucellosis

A 27-year-old man, recent visitor to the Middle East, presented with 6-week history of fever (up to 102°F) followed by altered behavior and left hemiparesis. CSF was acellular with raised protein (138 mg/dL). CSF bacterial culture was sterile; adenosine deaminase normal (3 U/L); cryptococcal antigen, Venereal Disease Research Laboratory test, and Japanese B serology were negative. HIV serology and vasculitic workup were unremarkable. Serum Brucella agglutination titer was 320 IU (immunoglobulin M fraction 280 IU). Cranial MRI showed nonenhancing bilateral white matter and basal ganglia hyperintensities on T2-weighted images (figure, A–C). The patient was treated with IV ceftriaxone (1 month) along with oral doxycycline and rifampicin (4 months). At 3 months, Brucella agglutination titer was <20 IU and the patient became independent. Follow-up imaging showed a reduction in lesions (figure, D). Brucellosis frequently presents as chronic meningitis along with cranial neuropathies and spinal arachnoiditis.1 Demyelinating lesions are described in neurobrucellosis,1,2 involvement of the deep gray matter being unusual.

Is Neurobrucellosis the Pandora's Box of Modern Medicine?

TO THE EDITOR—The recent article by Guven et al [1], titled “Neurobrucellosis: Clinical and Diagnostic Features,” sheds light on many important yet vexing issues in the clinical presentation, diagnosis, andmanagementofarelativelycommon zoonotic infection. The relevance of discussing this issue is understated by the lack of consensus in the diagnosis and management of neurobrucellosis, in combination with unchanged diagnostic and therapeutic approaches for brucellosis being practiced for decades.Wewould like to express our views regarding certain aspects in the diagnosis and management of neurobrucellosis. The widely followed diagnostic criteria overemphasizes the role of abnormal cerebrospinal fluid (CSF) (positive Brucella agglutination titer in any titer, isolation of Brucella from CSF, and abnormal CSF parameters) in the diagnosis of neurobrucellosis [2]. However, in resourcepoor settings such as ours, facilities for determination of CSF Brucella agglutination titers are sparse. Due to the long

Wall-eyed bilateral inter nuclear ophthalmoplegia with vertical gaze palsy

A 64-year-old woman, diabetic and hypertensive, presented with sudden onset painless diplopia and alteration of consciousness. She was drowsy with neurological examination revealing exotropia of both eyes in primary position with bilateral internuclear ophthalmoplegia on attempted horizontal gaze (Figure 1a). Pupils were normal bilaterally. Convergence, vertical saccades, pursuits and vestibular ocular reflexes were impaired. Cranial magnetic resonance imaging (MRI) showed an acute infarct in the midline of mesencephalic …

Teaching NeuroImages: Terson syndrome in cortical venous sinus thrombosis

An 18-year-old woman presented with headache, right focal seizures, and diminished vision in the left eye for 20 days. Fundus examination revealed bilateral papilledema with large premacular sub–internal limiting membrane and subhyaloid bleeding in the left eye (figure 1A). MRI brain showed hemorrhagic infarct in the left temporal lobe (figure 2, A and B). Magnetic resonance venography showed left transverse and sigmoid sinus thrombosis (figure 2C). A diagnosis of Terson syndrome1 (vitreous hemorrhage) was made. Procoagulant workup was negative and the patient improved with conservative management2 (figure 1B). Even though Terson syndrome has been reported with subarachnoid hemorrhage, its occurrence with cortical venous sinus thrombosis is rare.

Fatal disseminated neurobrucellosis.

A 59-year-old cattle breeder hailing from rural north western India presented with insidious onset and gradually progressive hoarseness of voice and painless dysphagia for 5 months followed by ascending paraparesis and hearing loss for 2 months. He had significant loss of weight with anorexia of 5 months duration. Physical examination revealed pallor, bilateral 7th, 8th, 9th, 10th and left 12th cranial nerve palsies with sensorimotor deficits in radicular distribution (L3-S4) and neck stiffness. Hemogram showed elevated erythrocyte sedimentation rate of 42 mm in …

Disseminated tuberculosis presenting as rapidly progressive dementia.

A 35-year-old right-handed man presented with complaints of holocranial nonthrobbing headache with apathy, executive dysfunction and reduced social interaction for the past 1 month. No relevant systemic symptoms were present. General physical and neurological examination was unremarkable. Hematological parameters were normal except for raised erythrocyte sedimentation rate (52 mm in first hour). Gad-enhanced magnetic resonance imaging (MRI) brain showed acute left thalamic infarct …

An unusual presentation of ulcerative colitis.

Ulcerative colitis (UC) may have diverse extraintestinal manifestations. Nutritional deficiencies, medications or immune-mediated epiphenomena are considered to be pathogenic mechanisms involved. We describe a case of a 56-year-old woman who presented with rapidly progressive tingling paraesthesias in both lower limbs followed by sensory ataxia, ascending spastic quadriparesis, urgency and urge incontinence of 3 months duration. She had an episode of bloody diarrhoea 1 month later for which a colonoscopy was carried out with colonic biopsy features revealing a diagnosis of UC. In view of lack of alternative aetiology, the posterolateral column disease in our patient was attributed to an extraintestinal manifestation of UC. She improved dramatically with a course of intravenous steroids followed by tapering dose of oral steroids and oral mesalamine for her UC. Although rare, UC should be considered in the differential diagnosis of posterolateral column disease of the spinal cord in the appropriate clinical scenario.

Facial nuclear degeneration on MRI in bulbar onset amyotrophic lateral sclerosis.

A 45-year-old male presented with progressive dysarthria and dysphagia for 1 year. Examination revealed bilateral facial (Figure 1A) and neck flexor weakness, with depressed gag and tongue fasciculations. Fasciculations, wasting and brisk reflexes were noted in upper limbs. Facial reflexes were not brisk, and pseudobulbar affect was not present. Bell’s …

Teaching NeuroImages: Reversible paradoxical lithium neurotoxicity

A 33-year-old man with bipolar affective disorder presented with acute onset of rigidity, tremors, and confusion. He had been taking oral lithium (1,200 mg daily) for the past 2 months. Baseline blood, EEG, and CSF analyses were normal. Serum lithium level was 0.67 mEq/L (0.3–1.3). Gadolinium MRI brain showed multiple bilateral symmetric T2-weighted hyperintensities (figure, A–C). On suspicion of lithium-induced neurotoxicity, lithium was replaced with valproate. At 1-month follow-up, his extrapyramidal symptoms had resolved completely, with significant resolution noted on cranial MRI (figure, D–F). Paradoxical lithium neurotoxicity occurs at therapeutic or low serum levels due to lithium-induced toxic demyelination.1-3

Acute Marchiafava-Bignami disease presenting as reversible dementia in a chronic alcoholic

Marchiafava-Bignami disease (MBD) is a rare complication of chronic alcoholism. Its clinical diagnosis has considerably changed during recent times, with MRI of the brain paving way for in life diagnosis. We believe that physicians need to have a high index of suspicion, because acute onset MBD is not always fatal and complete recovery is possible, provided the diagnosis is made early and treated appropriately. We report a case of MBD who was diagnosed early in the disease course with subsequent clinical and radiological recovery on institution of appropriate treatment.