Compensatory hyperhidrosis is a form of neuropathy. It is encountered in patients with myelopathy, thoracic disease, cerebrovascular disease, nerve trauma or after surgeries. The exact mechanism of the phenomenon is poorly understood. It is attributed to the perception in the hypothalamus (brain) that the body temperature is too high. The sweating is induced to reduce body heat. Excessive sweating due to nervousness, anger, previous trauma or fear is called hyperhidrosis. Compensatory hyperhidrosis is the most common side effect of endoscopic thoracic sympathectomy, a surgery to treat severe focal hyperhidrosis, often affecting just one part of the body. It may also be called rebound or  reflex hyperhidrosis. In a small number of individuals, compensatory hyperhidrosis following sympathectomy is disruptive, because affected individuals may have to change sweat-soaked clothing two or three times a day. According to Dr. Hooshmand, sympathectomy permanently damages the temperature regulatory system. The permanent destruction of thermoregulatory function of the sympathetic nervous system causes latent complications, e.g., RSD in contralateral extremity.Following surgery for axillary (armpit), palmar (palm) hyperhidrosis (see focal hyperhidrosis) and blushing, the body may sweat excessively at untreated areas, most commonly the lower back and trunk, but can be spread over the total body surface below the level of the cut. The upper part of the body, above the sympathetic chain transection, the body becomes anhidriotic, where the patient is unable to sweat or cool down, which further compromises the bodys thermoregulation and can lead to elevated core temperature, overheating and hyperthermia.
Signs and symptoms
People with intracerebral bleeding have symptoms that correspond to the functions controlled by the area of the brain that is damaged by the bleed. These localizing signs and symptoms can include hemiplegia (or weakness localized to one side of the body) and paresthesia (loss of sensation) including hemisensory loss (if localized to one side of the body). These symptoms are usually rapid in onset, sometimes occurring in minutes, but not as rapid as the symptom onset in ischemic stroke. Other symptoms include those that indicate a rise in intracranial pressure caused by a large mass (due to hematoma expansion) putting pressure on the brain. These symptoms include headaches, nausea, vomiting, a depressed level of consciousness, stupor and death. Continued elevation in the intracranial pressure and the accompanying mass effect may eventually cause brain herniation (when different parts of the brain are displaced or shifted to new areas in relation to the skull and surrounding dura mater supporting structures). Brain herniation is associated with hyperventilation, extensor rigidity, pupillary asymmetry, pyramidal signs, coma and death.Hemorrhage into the basal ganglia or thalamus causes contralateral hemiplegia due to damage to the internal capsule. Other possible symptoms include gaze palsies or hemisensory loss. Intracerebral hemorrhage into the cerebellum may cause ataxia, vertigo, incoordination of limbs and vomiting. Some cases of cerebellar hemorrhage lead to blockage of the fourth ventricle with subsequent impairment of drainage of cerebrospinal fluid from the brain.