الفهرس Only 14 pages are availabe for public view
 |  | from | 233 |  |  |
| | | from | 233 | | |
Abstract
There are certain neurological disorders that present with stroke and epilepsy together.
Two examples of these disorders are:
1-Mitochondrialmyopathy, encephalomyopathy, lactic acidosis, and strokelike episodes (MELAS).
2-Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL) would be discussed as an example.
Mitochondrial myopathy, encephalopathy, lactic acidosis and stroke-like episodes (MELAS) is the most common maternally inherited mitochondrial disease. The typical clinical manifestations of MELAS include stroke-like episodes, seizures, short stature, and encephalopathy and muscle weakness.
Stroke-like episodes constitute an important clinical manifestation of MELAS and are the age of onset of the stroke-like episodes is characteristically between 5 and 15 years. The clinical definition of a stroke-like episode includes both focal and non focal manifestations.
In a recent investigation, reported the occurrence of focal epileptiform discharges on electroencephalogram (EEG) in 80% of the stroke-like episodes in MELAS.
Radiological Characteristics of Stroke-Like Lesions in MELAS:
A distribution of the stroke-like lesions incongruent to a vascular territory
Preferential involvement of the cerebral cortex (bright thickened cortical band on T2-weighted and FLAIR images)
Predilection to the posterior brain
Reversible vasogenic edema
Slowly progressive spread into the surrounding cortex
T1-weighted cortical hyperintense signal during subacute stage
compatible with cortical laminar necrosis pattern
Epilepsy is a common feature in the MELAS syndrome. Management of seizures typically involves the use of phenobarbital (phenobarbitone), phenytoin, carbamazepine, gabapentin, lamotrigine, benzodiazepines and zonisamide.
Riboflavin (vitamin B2) is functioning as a cofactor for electron transport in complex I, complex II and the electron transfer flavoprotein.
The rationale for nicotinamide treatment in patients with the MELAS syndrome is that the substrate affinity of complex I may be diminished in this condition and could be counter balanced by increasing the mitochondrial NAD+ level.
Cerebral autosomal dominant leukoencephalopathy, arteriopathy with subcortical infarcts and appears to be the most common form of hereditary stroke disorder CADASIL is associated with arterial smooth muscle degeneration linked to mutations in the Notch3 gene, whose product is a transmembrane receptor. Cerebral MRI reveals white matter and microangiopathic pattern of signal abnormalities suggestive of ischaemic infarcts, lacunes and diffuse leukoencephalopathy that are located within the periventricular white matter, the basal ganglia, the thalamus, the internal capsule and the pons. Seizures after stroke are classified as early or late onset, according to their timing after brain ischemia, in a paradigm comparable to post-traumatic epilepsy .An arbitrary cut point of 2 weeks after the presenting stroke has been recognized to distinguish between early- and late-onset poststroke seizures.
Cortical location is among the most reliable risk factors for poststroke seizures. Poststroke seizures were more likely to develop in patients with larger lesions involving multiple lobes of the brain than in those with single lobar involvement.
The mechanism of seizure initiation by hemorrhage is not established. Products of blood metabolism, such as hemosiderin, may cause a focal cerebral irritation leading to seizures.