Joe James

Postpartum Woman With Seizures

A 27-year-old woman, postpartum day 9, presented with sudden onset of headache, vomiting, visual blurring, and 3 episodes of generalized tonic-clonic seizures. She had had an uneventful cesarean delivery 9 days previously and was discharged home. Her antenatal period was uneventful, and she did not have gestational hypertension. On examination, she was alert, oriented, and afebrile. Her blood pressure was 150/100 mm Hg, which had increased from her mean antenatal recording of 130/80 mm Hg. Fundus examination result was normal, and there were no focal neurologic deficits. Magnetic resonance imaging (MRI) of the brain showed T2 and T2 fluid-attenuated inversion recovery (FLAIR) hyperintense signals in bilateral parietooccipital lobes (Figures 1 and 2) and bilateral cerebellar hemispheres (Figure 3), without any diffusion restriction. She was treated with intravenous labetalol, nifedipine, and fosphenytoin. Her blood pressure normalized and her symptoms subsided, and she was later discharged.

Acute Necrotizing Vasculitic Neuropathy due to Polyarteritis Nodosa

Necrotizing vasculitic neuropathy in polyarteritis nodosa can rarely present acutely and may mimic acute inflammatory neuropathies. A 53-year-old male presented with an acute neurological illness characterized by paresthesia and weakness of both lower limbs lasting six-days. He also had mild paresthesia of both hands. On examination, there were confluent, purpuric, and ecchymotic patches over the extensor aspects of both lower limbs, which were palpable. Neurological examination revealed grade II/V power with hypotonia and absent reflexes in the lower limbs. All modalities of sensation were decreased below the knee. Sensory impairment was also noted on the fingertips of both hands. Nerve conduction study suggested an asymmetrical sensorimotor axonal neuropathy. Sural nerve biopsy was consistent with necrotizing vasculitis. He was treated with intravenous methylprednisolone followed by oral prednisolone and monthly cyclophosphamide injection for six-months and made a good recovery.

Herpes Simplex Virus Encephalitis in a Healthy Lady

The case describes a middle aged lady with herpes simplex encephalitis. The highlight of the case is the MRI which depicts all the typical features of herpes encephalitis. Herpes virus is the most common cause of encephalitis worldwide. It is very important to recognize this typical MRI picture and initiate Acyclovir therapy at the earliest because, early initiation of therapy is the single factor which affects the prognosis of this serious neurological illness.

Central nervous system tuberculosis – The gray area in tuberculosis treatment

Hydrocephalus is the most common complication of TBM. This occurs due to the basal exudates and inflammation leading to fibrosis and aqueductal obstruction and is usually obstructive type but may also be communicating type. The usual treatment for hydrocephalus, ventriculoperitoneal (VP) shunting should not be the first line in TBM hydrocephalus. Shunt obstruction and secondary infection are common in the setting of TBM and lead to high mortality and morbidity. In a study of 65 patients treated with VP shunt for TBM, the complication rate was as high as 32.3%.[5] Hence, VP shunt in hydrocephalus due to TBM should be reserved for cases resistant to medical therapy.

Ring enhancing lesions in the brain of an HIV infected patient: a diagnostic challenge

A 58-year old male presented with headache, unsteadiness of gait and cognitive decline in the form of loss of recent memory of 1-month duration. He also reported significant loss of weight. Neurological examination revealed short term memory loss and gait apraxia. There were no cerebellar signs or sensorimotor deficits. He was tested positive for HIV. MRI showed T2-FLAIR hyperintense lesions with edema in the left centrum semiovale (A), right basal ganglia (B) and right frontal corticomedullary junction (C). The corresponding lesions in T1 after gadolinium showed ring enhancement (D-F). His CD4 count was 70/?L. Serum IgG Toxoplasma was positive. He was started on pyrimethamine with sulfadiazine and anti-retroviral treatment and discharged. Toxoplasmosis is a parasitic infection caused by Toxoplasma gondii. CNS Toxoplasmosis is an important differential diagnosis in HIV patients presenting with neurological symptoms. Common presentations are headache, seizures, focal neurological deficits like hemiparesis or aphasia, and altered sensorium. Toxoplasmosis in AIDS is due to reactivation of previously acquired infection as immunity wanes, almost always when CD4 count is less than 100/?L. Multiple ring enhancing lesions in the corticomedullary junctions of frontal and parietal lobe, centrum semiovale and basal ganglia with edema and mass effect in an HIV patient is virtually diagnostic of toxoplasmosis. Ring enhancing lesions in the brain can also be seen in primary CNS lymphoma which often causes diagnostic confusion. An isolated ring enhancing lesion larger than 4cm in size or a positive serology for Ebstein-Barr virus in CSF favors lymphoma over toxoplasmosis.

Progressive dementia with seizures in an HIV infected lady

A 40-year-old female presented with progressive memory loss over the past 1-month. She had one episode of generalized tonic clonic seizure 2-months back, but did not take any treatment. She had significant involuntary weight loss. On examination she was emaciated and had a BMI of 16.4. Neurological examination showedcognitive decline in the form of loss of recent memory,judgment and abstract thinking, with preserved language and visuospatial orientation. There were no focal neurological deficits. She was tested positive for HIV. Her CD4+ count was 21/µL. Computed tomographyof the brain revealed bilateral hypodensities in the periventricular area (A). MRI of the brain showed bilateral symmetrical periventricular white matter FLAIR hyperintensities in frontal and parietal lobes with diffuse brain atrophy suggestive of HIV encephalopathy (B). She was started on combination antiretroviral therapy with tenofovir, lamivudine and efavirenz and discharged. HIV encephalopathy refers to neurocognitive disorders associated with HIV infection. It usually occurs in late stages of HIV-infection and correlates with advanced immunosuppression. Earliest recognizable findings include impairment of attention and concentration. This progresses to frank dementia, personality changes and motor abnormalities. Neuroimaging typically shows global cerebral atrophy with symmetrical white matter hyperintensities predominantly in the periventricular area. Lesions of progressive multifocal leukoencephalopathy can mimic HIV encephalopathy, but are usually asymmetric, involve the peripheral “U” fibres first and have predilection for parieto-occipital lobes.Treatment of HIV encephalopathy is initiation or intensification of anti-retroviral therapy, and psychomotor improvement is usually seen after therapy.

Cerebral venous thrombosis after intravenous immunoglobulin therapy in immune thrombocytopenic purpura

A common misconception is that immune thrombocytopenic purpura (ITP) causes only bleeding diathesis. From this case vignette of a young male with ITP who had cerebral venous thrombosis, we highlight the importance of considering venous thrombosis in such patients when they present with focal cerebral signs.

Idiopathic intracranial hypertension with spontaneous cerebrospinal fluid leak into the orbit

from the posterior end of the optic nerve sheath. The high intracranial pressure might have caused the CSF around the optic nerve to leak and form an encapsulated collection outside the optic nerve. CSF leaks are well described in IIH. Spontaneous CSF rhinorrhea and otorrhea can occur in IIH.[1,2] Such leaks provide a natural mechanism for reducing intracranial pressure, and papilledema is much less common in such cases. In our case, the leak was not manifested exteriorly but internally into the orbit. Optic nerve fenestration is one of the surgical treatments of IIH to reduce the risk of visual loss.[3] We can consider our case as a natural, spontaneous fenestration where CSF escaped A 50-year-old male with chronic inflammatory demyelination polyneuropathy (CIDP) on treatment with deflazacort for over a year presented with insidious onset headache of 3-month duration. The headache was diffuse and was not aggravated by coughing or straining. He did not have any early morning headache, transient visual obscurations, or tinnitus. He was diagnosed to have CIDP 1-year back and had a good response to deflazacort and was advised to continue the treatment. Physical examination revealed swelling of the superolateral aspect of both eyeballs. There was no proptosis, chemosis, or restriction of extraocular movements. Fundus examination showed bilateral papilledema. The magnetic resonance imaging of brain showed linear tortuous T1 hypointense and T2 hyperintense lesion in both orbits [Figure 1]. The lesion was encapsulated, running parallel to the optic nerve in the extraconal space and was connected to the optic nerve sheath near the orbital apex [Figure 2]. There was also a partial empty sella. A lumbar puncture measured an opening pressure of 240 mm of cerebrospinal fluid (CSF). CSF protein was 84 mg/dl, sugar 68 mg/dl, without any cells, and culture was sterile. The patient had immediate relief of headache after removal of 20 ml of CSF. The usual causes of idiopathic intracranial hypertension (IIH) such as obesity, antibiotic use, autoimmune disorders, and thyroid dysfunction were ruled out. A diagnosis of IIH secondary to chronic steroid use was made.