Non-convulsive status epilepticus presenting with wernick's aphasia

Ictal aphasia in adults is a rare phenomenon. Most reported cases manifest with non-fluent [Broca] aphasia. Ictal fluent [Wernicke] aphasia is less common. We report a 47-year-old, right-handed woman that presented with recurrent episodes of non-convulsive seizures in the form of Wernickes aphasia for 2 weeks. An MRI of the brain showed an old cerebral infarction in the left parieto-occipital area. Scalp EEG revealed continuous periodic sharp waves at the left temporal regions with diffusion to the whole left hemisphere and at occasions to the right. This is followed by variable periods of post ictal slowing. Recurrence of the described ictal pattern was noted. Management of status epilepticus was started in the form of intravenous diazepam and a loading dose of phenytoin and phenobarbitone. After treatment, she improved clinically and the EEG improved with disappearance of the left temporal ictal rhythm and normalization of the EEG background. Thus, establishing the diagnosis of non-convulsive partial status epilepticus manifesting as ictal aphasia

fatal pseudallescheria boydii brain abscess

We present the clinical and radiological features of pseudallescheria boydii infection in a middle aged woman who presented with right frontal pseudallescheria abscess after two years use of prednisolone for rheumatoid arthritis. Despite early surgical excision and intravenous antifungal treatment she died after 7 weeks despite aggressive therapy

Neurobiology and pathogenesis of alzeimer's disease

Recently, an evolution occurred in understanding of basic pathophysiological mechanism in Alzheimer's disease. The exact etiology of Alzheimer's disease is undetermined, several factors are associated with increased or decreased risk of developing Alzheimer's disease. Risk factors include several genetic mutations that are associated with familial Alzheimer's disease such as genetic mutations on chromosomes 21, 14, 1, Ellele 4 on epolipoprotein gene EP[o]E4 and others. Other risk factors include advanced age, female gender, smaller head circumference, previous head trauma, family history and possibly low intelligence or low education. Exposure to risk factors stimulates the neuropathological cascade of Alzheimer's disease which includes structural changes and alteration of the neurotransmitter pathways. The structural changes include formation of neuritic plaques and neurofibrillary tangles. Neuritic plasques and neurofibrillary tangles together represent the histopathological hallmarks of Alzheimer's disease. As a consequence of neuritic plaques and neurofibrillary tangles formations synaptic loss and neuronal death occurs and subsequently the neurotransmitter pathwaysalter. The main neurotransmitter affected is acetylcholine, as degeneration of the basal nucleus of Meynert and its projection to the temporal 1obe and basal forebrain occurs. The alteration of cholinergic pathwasy correlates with cognition decline in Alzheimer's disease. At the actylcholine receptors, reduced synthesis of choline acety-1 transferase enzyme occurs. This enzyme is produced by the basal mucleus of meynert. There is reduction of the muscurinic presynaptic M2 receptors and there is reduced acetylcholine transports. These structural changes start in the medial temporal lope and basal forebrain and progress in the vulnerable regions namely: temporal lobes, basal forebrain, basal nucleus of Meynert, locus ceruleus and dorsal Raphael nuclei. The thalamus, basal ganglia, brainstem, cerebellum and primary sensory and motor cortex are minimally involved. Serotoninergic pathway alteration correlates with the behaviour changes in Alzheimer's disease. Other neurotransmitter alterations include noradrenergic, glutamatergic, somatostatin and GABA pathways. Understanding the pathological cascade in Alzheimer's disease provide the basis of therapeutic opportunities. In the following syllabus, we discuss the neurobiology, pathogenesis and neuropathological cascade of Alzheimer's disease