What is Dysautonomia? Dysautonomia refers to a disorder of autonomic nervous system (ANS) function.

Most physicians view dysautonomia in terms of failure of the sympathetic or parasympathetic components of the ANS, but dysautonomia involving excessive ANS activities also can occur. Dysautonomia can be local, as in reflex sympathetic dystrophy, or generalized, as in pure autonomic failure. It can be acute and reversible, as in Guillain-Barre syndrome, or chronic and progressive. Several common conditions such as diabetes and alcoholism can include dysautonomia. Dysautonomia also can occur as a primary condition or in association with degenerative neurological diseases such as Parkinson's disease. Other diseases with generalized, primary dysautonomia include multiple system atrophy and familial dysautonomia. Hallmarks of generalized dysautonomia due to sympathetic failure are impotence (in men) and a fall in blood pressure during standing (orthostatic hypotension). Excessive sympathetic activity can present as hypertension or a rapid pulse rate. Is there any treatment? There is no cure for dysautonomia. Secondary forms may improve with treatment of the underlying disease. In many cases treatment of primary dysautonomia is symptomatic and supportive. Measures to combat orthostatic hypotension include elevation of the head of the bed, frequent small meals, a high-salt diet, and drugs such as fludrocortisone, midodrine, and ephedrine. What is Holmes-Adie syndrome ? Holmes-Adie syndrome (HAS) is a neurological disorder affecting the pupil of the eye and the autonomic nervous system. It is characterized by one eye with a pupil that is larger than normal and constricts slowly in bright light (tonic pupil), along with the absence of deep tendon reflexes, usually in the Achilles tendon. HAS is thought to be the result of a viral or bacterial infection that causes inflammation and damage to neurons in the ciliary ganglion, an area of the brain that controls eye movements, and the spinal ganglion, an area of the brain involved in the response of the autonomic nervous system. HAS begins gradually in one eye, and often progresses to involve the other eye. At first, it may only cause the loss of deep tendon reflexes on one side of the body, but then progress to the other side. The eye and reflex symptoms may not appear at the same time. People with HAS may also sweat excessively, sometimes only on one side of the body. The combination of these 3 symptoms abnormal pupil size, loss of deep tendon reflexes, and excessive sweating is usually called Rosss syndrome, although some doctors will still diagnosis the condition as a variant of HAS. Some individuals will also have cardiovascular abnormalities. The HAS symptoms can appear on their own, or in association with other diseases of the nervous system, such as Sjogrens syndrome or migraine. It is most often seen in young women. It is rarely an inherited condition.

Is there any treatment? Doctors may prescribe reading glasses to compensate for impaired vision in the affected eye, and pilocarpine drops to be applied 3 times daily to constrict the dilated pupil. Thoracic sympathectomy, which severs the involved sympathetic nerve, is the definitive treatment for excessive sweating. Babinski's sign I A pathological reflex where the great toe extends and flexes toward the top of the foot and the other toes fan out when the sole of the foot is firmly stroked. Normally, the great toe is flexed when the sole of the relaxed foot is stroked. Babinskis reflex is normal in children up to about two years of age. The persistence in older people is a sign of damage to the corticospinal tract. Because this tract is right- and left-sided, a Babinskis reflex can occur on one side or on both sides. An abnormal Babinskis reflex can be temporary or permanent. The test for Babinskis sign, called Babinskis test, is running a pointed instrument up the lateral border of the foot and crossing to the medial side over the metatarsal pads. The term Babinskis sign also refers to a reflex of the forearm and indicates a lesion of the spinal cord. Flix Alfred Vulpian, neuropathologist at the Hpital de Salptrire in Paris, half a century before Babinski had observed the extension of the great toe in certain types of brain damage. The sign had also been reported three years before by Ernst Julius Remak (1849-1911), but it was Babinski who first realized its diagnostic significance. In 1896, at a meeting of the Socit de Biologie, Babinski first reported his discovery that while the normal reflex of the sole of the foot consists of a plantar reflex of the toes; an injury to the pyramidal tract will show up in an isolated dorsal flexion of the great toe. In 1903 he completed his report with another article containing a description of the fanning of the other toes.