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Focal neurological deficits may be caused by a variety of medical conditions such as head trauma, [1] tumors or stroke; or by various diseases such as meningitis or encephalitis or as a side effect of certain medications such as those used in anesthesia. [2] Neurological soft signs are a group of non-focal neurologic signs. [3]
Lateral temporal lobe seizures arising from the temporal-parietal lobe junction may cause complex visual hallucinations. [2] In comparison to mesial temporal lobe seizures, lateral temporal lobe seizures are briefer duration seizures, occur with earlier loss of awareness, and are more likely become a focal to bilateral tonic-clonic seizure. [ 2 ]
This is a list of major and frequently observed neurological disorders (e.g., Alzheimer's disease), symptoms (e.g., back pain), signs (e.g., aphasia) and syndromes (e.g., Aicardi syndrome). There is disagreement over the definitions and criteria used to delineate various disorders and whether some of these conditions should be classified as ...
Focal means that it is limited to a focal zone in any lobe. [2] Focal cortical dysplasia is a common cause of intractable epilepsy in children and is a frequent cause of epilepsy in adults. There are three types of FCD with subtypes, including type 1a, 1b, 1c, 2a, 2b, 3a, 3b, 3c, and 3d, each with distinct histopathological features.
If a focal seizure spreads from one hemisphere to the other side of the brain, this will give rise to a focal to bilateral seizure. [5] [6] The person will become unconscious and may experience a tonic–clonic seizure. Individuals with multiple focal seizures typically have a condition known as temporal lobe epilepsy.
Geschwind syndrome, also known as Gastaut–Geschwind syndrome, is a group of behavioral phenomena evident in some people with temporal lobe epilepsy.It is named for one of the first individuals to categorize the symptoms, Norman Geschwind, who published prolifically on the topic from 1973 to 1984. [1]
However, as self-monitoring and somatic marker processes are so complex, it likely involves other brain regions. Therefore, neuropsychological tests are sensitive to the dysfunction of orbitofrontal cortex, yet are not specific to it. The weakness of these tests is that they do not necessarily show dysfunction of the orbitofrontal cortex.
The associated autobiographical memory impairment is, however, a more puzzling consequence of medial temporal lobe pathology on this theory. It could be that epileptiform activity originating in the medial temporal lobe has the potential to disrupt the distributed neocortical traces required to maintain detailed autobiographical memories.