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The treatment of cerebral edema depends on the cause and includes monitoring of the person's airway and intracranial pressure, proper positioning, controlled hyperventilation, medications, fluid management, steroids. [3] [7] [8] Extensive cerebral edema can also be treated surgically with a decompressive craniectomy. [7]
Lateral temporal lobe seizures arising from the temporal-parietal lobe junction may cause complex visual hallucinations. [2] In comparison to medial 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]
Limbic encephalitis is a rare condition with no randomised-controlled trials to guide treatment. Treatments that have been tried include intravenous immunoglobulin, plasmapheresis, corticosteroids, cyclophosphamide and rituximab. [1] If an associated tumour is found, then recovery is not possible until the tumour is removed.
In uncal herniation, a common subtype of transtentorial herniation, the innermost part of the temporal lobe, the uncus, can be squeezed so much that it moves towards the tentorium and puts pressure on the brainstem, most notably the midbrain. [8] The tentorium is a structure within the skull formed by the dura mater of the meninges.
[2] [3] Causes of a primary CSF leak are those of trauma including from an accident or intentional injury, or arising from a medical intervention known as iatrogenic. A basilar skull fracture as a cause can give the sign of CSF leakage from the ear, nose or mouth. [4] A lumbar puncture can give the symptom of a post-dural-puncture headache.
The swelling is worst at around four to six days after the injury. [3] Extensive contusion associated with subdural hematoma is called burst lobe. [5] Cases of a burst frontal or temporal lobe are associated with high mortality and morbidity. [5]
The olfactory nerve may also be involved in HSE, [12] which may explain its predilection for the temporal lobes of the brain, as the olfactory nerve sends branches there. In horses, a single-nucleotide polymorphism is sufficient to allow the virus to cause neurological disease; [13] but no similar mechanism has been found in humans.
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 ...