Examination And Investigations

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Two electroencephalograms (EEGs) showed ictal discharges from the right frontotem-poral region, but a subsequent 24-h ambulatory EEG was normal. Magnetic resonance imaging (MRI) scanning of the brain showed right hippocampal atrophy with a high T2 signal.

The patient received valproate for 2 months, and he seemed to improve during that time. Meanwhile, his diabetes worsened, blood glucose levels fluctuating between 0.5 and 3.5 g/l were noted and insulin was started. He continued to have both hypoglycemic episodes as well as marked hyperglycemic episodes. The amnestic episode was thought to be caused by transient hypoglycemia at that time, which could not be confirmed later with concomitant measurements.

The patient was seen in our hospital in May 1997 for evaluation of a few further similar episodes. A first EEG captured some slow spikes as well as a "subclinical" right temporal lobe seizure on a later, standard EEG whose interpretation was uncertain. Nonetheless, vigabatrin was added to valproate. The amnestic episodes were infrequent during the following 6 months (occurring about once every 2 months), and they happened during periods of normal or high blood glucose levels.

FIGURE 28.1 MRI coronal image of a FLAIR sequence, perpendicular to the long axis of hippocampus, at day 11 of an amnestic simple partial status epilepticus. The left hippocampus is swollen and hyperintense. The atrophy of the right hippocampus is known and seems stable since the beginning of the epilepsy.

FIGURE 28.1 MRI coronal image of a FLAIR sequence, perpendicular to the long axis of hippocampus, at day 11 of an amnestic simple partial status epilepticus. The left hippocampus is swollen and hyperintense. The atrophy of the right hippocampus is known and seems stable since the beginning of the epilepsy.

In October 1997, the events shortened to a few minutes but increased dramatically in frequency, leading to a quasi-permanent amnestic state in which both anterograde and retrograde memories were affected. The patient was able to retain only very small amounts of information. He complained of gait trouble, behavioral changes, and a mild temporal-spatial disorientation. EEGs established a definite diagnosis of simple partial status epilepticus, showing temporal lobe seizures on both sides independently (but predominantly on the left). Up to three events in 30 min were recorded. Each seizure remained largely confined to one temporal lobe, although they would propagate mildly to neighboring regions without any further clinical symptomatology. There was no evidence of impairment of consciousness. On admission the cerebrospinal fluid (CSF) was found to contain 0.4 g/l of protein, normal cell count, and normal glucose levels (the patient was hyperglycemic at that time). Interferon-a was undetectable. The CSF remained normal 3 days and 1 week later. Herpes simplex virus-1 antibodies and the polymerase chain reaction were negative in the CSF. Other laboratory tests (including virology, bacteriology, autoimmunity and inflammatory, and paraneoplastic markers) were negative.

The seizures remained very active for 2 weeks despite clonazepam followed by intravenous phenytoin, together with high doses of oral antiepileptic drugs in combination (valproate, phenytoin, vigabatrin, and clonazepam). Over the next 2 weeks the seizures disappeared, as shown by EEG monitoring. A brain MRI at day 11 of admission showed a swollen and T2-hypertintense left amygdalo-hippocampal complex with an unchanged right hippocampus (Figure 28.1). Despite the resolution of the status epilepticus, the amnestic and behavioral symptoms regressed slightly and partially during the 2 months of hospitalization. A series of brain MRIs showed: at day 42 of arrival, decreased swelling on the left side; 3 months later, disappearance of swelling and evolution into a notable hippocampal atrophy on the left side and an increase of right hip-pocampal atrophy (Figure 28.2). The latest MRI (November 1998) confirmed bilateral hippocampal atrophy.

FIGURE 28.2 Coronal slice of a T2-weighted MRI scan perpendicular to the long axis of hippocampus, 5 months after the occurrence of an amnestic simple partial status epilepticus. The left hippocampus is dramatically atrophic and the right hippocampus (originally affected) also showed a notable loss of volume.

FIGURE 28.2 Coronal slice of a T2-weighted MRI scan perpendicular to the long axis of hippocampus, 5 months after the occurrence of an amnestic simple partial status epilepticus. The left hippocampus is dramatically atrophic and the right hippocampus (originally affected) also showed a notable loss of volume.

The clinical evolution was poor, with persistent anterograde amnesia, spatial-temporal disorientation, and behavioral disorders with disinhibition and joviality.

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Diabetes 2

Diabetes 2

Diabetes is a disease that affects the way your body uses food. Normally, your body converts sugars, starches and other foods into a form of sugar called glucose. Your body uses glucose for fuel. The cells receive the glucose through the bloodstream. They then use insulin a hormone made by the pancreas to absorb the glucose, convert it into energy, and either use it or store it for later use. Learn more...

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