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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]
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 ...
This is a shortened version of the sixth chapter of the ICD-9: Diseases of the Nervous System and Sense Organs. It covers ICD codes 320 to 389 . The full chapter can be found on pages 215 to 258 of Volume 1, which contains all (sub)categories of the ICD-9.
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 ]
The abnormal electrical activity might spread to the rest of the brain and cause a focal to bilateral seizure or a generalized tonic–clonic seizure. [20] The newer classification of 2017 groups only focal and generalized seizures, and generalized seizures are those that involve both sides of the brain from the onset. [6] [5]
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.
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.
In 1825, Bouchet and Cazauvieilh described palpable firmness and atrophy of the uncus and medial temporal lobe of brains from epileptic and non-epileptic individuals. [4]: 565 In 1880, Wilhelm Sommer investigated 90 brains and described the classical Ammon's horn sclerosis pattern, severe neuronal cell loss in hippocampal subfield cornum Ammonis 1 (CA1) and some neuronal cell loss in ...