Central Nervous System Infections « HKU E-learning Platform in Clinical Neurosciences

Archive for the ‘Central Nervous System Infections’ Category

Viral Encephalitis

Thursday, August 21st, 2014

Herpes simplex encephalitis

Viral encephalitis is a serious neurological disorder associated with relatively poor outcome. Herpes simplex virus (HSV) encephalitis is the most common causative agent for viral encephalitis. More than 95% of HSV encephalitis is caused by HSV type 1. HSV 1 is transmitted primarily via saliva which subsequently enters the oral mucosa and spreads to the ganglia nearby (trigeminal, superior and inferior cervical ganglia most common). Initially the virus is latent in the trigeminal ganglion. However, reactivation of the virus could occur spontaneously or could be triggered by trauma, stress, immunosuppression, or hormonal fluctuations.

Upon reactivation, there would be intracranial spread of the virus along the small meningeal braches of the trigeminal nerve, affecting the temporal lobe and orbital surface of the frontal lobe, which are the most common regions affected. The series of MRI scans here are taken from a middle-aged patient who presented with a few day history of fever and confusion (Figures 1 to 6). Lumbar puncture showed a lymphocytic predominant pleocytosis with normal CSF protein and glucose levels. Polymerase chain reaction for HSV-1 was positive. A cranial MRI subsequently demonstrated hyperintensities over bilateral temporal lobes (right more than left) in the T2W scan (axial cuts, Figures 1 and 2) as well as the FLAIR sequences (coronal cuts, Figures 5 and 6). There was also evidence of restricted diffusion over both temporal lobes (Figures 3 and 4). The patient was promptly started on intravenous acyclovir after suspicion of a central nervous system infection and continued for a total of fourteen days after confirmation by viral PCR.

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Tags:CNS infection, Encephalitis, Herpes simplex encephalitis, Japanese B encephalitis, Viral encephalitis
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Cerebral Abscess

Thursday, August 21st, 2014

The scans shown are from two immunocompromised patients who presented with high fever and recurrent seizures. The contrast cranial CT of the first patient shows that the patient had a rim-enhancing lesion at the left basal ganglia (Figure 1). A set of cranial MRIs of the second patient also showed multiple contrast enhancing lesions in the right basal ganglia and also a larger one at the left parietal lobe (Figures 2 and 3).

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Tags:Cerebral abscess, CNS infection
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Toxoplasmosis

Thursday, August 21st, 2014

The set of cranial MRI (coronal cuts) shown here are from a patient presenting with fever and confusion. Multiple, ring-enhancing nodular lesions are noted in the FLAIR sequence (Figures 1 and 2) as well as in the T1W imaging with contrast (Figures 3 and 4). Serology was positive for toxoplasma and the patient was tested to be HIV positive.

Toxoplasmosis is caused by the intracellular parasite Toxoplasma gondii. Although any mammal can be a carrier of the parasite and thus act as an intermediate host, cats are the definitive host. Humans become infected when the organism is accidentally ingested.

CNS toxoplasmosis most commonly involves the basal ganglia, thalami, grey-white matter junctions and cerebellum. Lesions are often multifocal and most lesions are small, averaging 2-3cm in diameter.

Toxoplasmosis of the central nervous system is the leading cause of focal central nervous system disease in patients with AIDS with primary central nervous system lymphoma being a major differential diagnosis. However, in contrast to toxoplasmosis, primary CNS lymphomas are often solitary. Lesions are located at the basal ganglia and deep white matter, often abutting the lateral ventricles and crossing the corpus callosum.

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Tags:CNS infection, Toxoplasmosis
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Creutzfeld-Jakob Disease

Thursday, August 21st, 2014

Creutzfeld-Jakob Disease (CJD) are prion diseases and can be subdivided into sporadic (account for 85% of cases), genetic (15% of cases) and acquired forms (<1% cases). CJD is rare with an incidence of 1-1.5 per million population per year with a peak age of onset of 55-75years. It is a common cause of rapidly progressive dementia. However, other symptoms including myoclonus, visual or cerebellar disturbances, pyramidal and extrapyramidal signs are also common and these occur depending on where the abnormal prion proteins accumulate in the brain. Investigations such as electroencephalogram (showing the classical 1 cycle per second spike and wave discharge), presence of 14-3-3 protein, neuron-specific enolase and total tau in the CSF only have moderate sensitivities in patients with CJD. In contrast, the presence of abnormal hyperintensity in the cortical gyri (“cortical ribboning”) is shown to be present in 98% of CJD patients and can be seen in the set of MRI images (diffusion weighted imaging sequence) shown here (Figures 1 to 4, especially prominent in the right temporal, parietal and occipital lobe cortices in this case). The management of patients with CJD is mainly supportive. The prognosis is extremely poor, and patients often deteriorate into an “akinetic-mutism” state at the end stage of the disease. The mean survival from onset of neurological symptoms is approximately 4 months.