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The basal ganglia is a collective group of structures in the brain. These include the striatum, (composed of the putamen and caudate nucleus), globus pallidus, substantia nigra, and the subthalamic nucleus. Along with other structures, the basal ganglia are part of a neural circuit that is integral to voluntary motor function. [1]
Hemiballismus or hemiballism is a basal ganglia syndrome resulting from damage to the subthalamic nucleus in the basal ganglia. [1] It is a rare hyperkinetic movement disorder, [2] that is characterized by pronounced involuntary limb movements [1] [3] on one side of the body [4] and can cause significant disability. [5]
Encephalitis with meningitis is known as meningoencephalitis, while encephalitis with involvement of the spinal cord is known as encephalomyelitis. [ 2 ] The word is from Ancient Greek ἐγκέφαλος , enképhalos 'brain', [ 37 ] composed of ἐν , en , 'in' and κεφαλή , kephalé , 'head', and the medical suffix -itis 'inflammation'.
The basal ganglia, also called basal nuclei, are a set of structures deep within the hemispheres involved in behaviour and movement regulation. [28] The largest component is the striatum, others are the globus pallidus, the substantia nigra and the subthalamic nucleus. [28]
The brain stem is involved in maintaining basic life functions such as breathing, swallowing, and circulation; the basal ganglia and cerebellum control movement and balance. Damage to these areas therefore results in the major symptoms of Leigh syndrome—loss of control over functions controlled by these areas. [1]
Autoimmune encephalitis (AIE) is a type of encephalitis, and one of the most common causes of noninfectious encephalitis. It can be triggered by tumors , infections , or it may be cryptogenic . The neurological manifestations can be either acute or subacute and usually develop within six weeks.
Neurodegeneration with brain iron accumulation is a heterogenous group of inherited neurodegenerative diseases, still under research, in which iron accumulates in the basal ganglia, either resulting in progressive dystonia, parkinsonism, spasticity, optic atrophy, retinal degeneration, neuropsychiatric, or diverse neurologic abnormalities. [1]
Another variant of ADEM in adults has been described, also related to anti-MOG auto-antibodies, has been named fulminant disseminated encephalomyelitis, and it has been reported to be clinically ADEM, but showing MS-like lesions on autopsy. [19] It has been classified inside the anti-MOG associated inflammatory demyelinating diseases. [58]