While most cases are due to bleeding from small aneurysms, larger aneurysms (which are less common) are more likely to rupture. Aspirin also appears to increase the risk.In 15–20 percent of cases of spontaneous SAH, no aneurysm is detected on the first angiogram. About half of these are attributed to non-aneurysmal perimesencephalic hemorrhage, in which the blood is limited to the subarachnoid spaces around the midbrain (i.e. mesencephalon). In these, the origin of the blood is uncertain. The remainder are due to other disorders affecting the blood vessels (such as cerebral arteriovenous malformations), disorders of the blood vessels in the spinal cord, and bleeding into various tumors.Cocaine abuse and sickle cell anemia (usually in children) and, rarely, anticoagulant therapy, problems with blood clotting and pituitary apoplexy can also result in SAH. Dissection of the vertebral artery, usually caused by trauma, can lead to subarachnoid hemorrhage if the dissection involves the part of the vessel inside the skull. Pathophysiology
Cerebral vasospasm is one of the complications caused by subarachnoid hemorrhage. It usually happens from the third day after the aneurysm event, and reaches its peak on 5th to 7th day. There are several mechanisms proposed for this complication. Blood products released from subarachnoid hemorrhage stimulates the tyrosine kinase pathway causing the release of calcium ions from intracellular storage, resulting in smooth muscle contraction of cerebral arteries. Oxyhaemoglobin in cerebrospinal fluid (CSF) causes vasoconstriction by increasing free radicals, endothelin-1, prostaglandin and reducing the level of nitric oxide and prostacyclin.
Antihistamines are a commonly prescribed first-line treatment for conventional urticaria, but its effectiveness in the treatment of CU is rather limited in most cases. Some research suggests that first-generation antihistamines with anticholinergic properties such as diphenhydramine are most successful at treating CU. Treatment(s) with mixed success: omalizumab (anti-IgE therapy), danazol (synthetic androgen), propranolol (beta blocker), zileuton (antileukotriene). Acquired anhidrosis and/or hypohidrosis
This subtype of CU refers to those who have abnormally reduced sweating. Diagnosis
Sweat is readily visualized by a topical indicator such as iodinated starch or sodium alizarin sulphonate. Both undergo a dramatic colour change when moistened by sweat. A thermoregulatory sweat test evaluates the bodys response to a thermal stimulus by inducing sweating through the use of a hot box ⁄ room, thermal blanket or exercise. Failure of the topical indicator to undergo a colour change during thermoregulatory sweat testing can indicate anhidrosis and/or hypohidrosis (see Minor test).A skin biopsy may reveal cellular infiltrates in sweat glands or ducts. Features
Severe heat intolerance (e.g., nausea, dizziness, and headache), and tingling, pricking, pinchy or burning pain over the entire body on exposure to hot environments or prolonged exercise which improve after cooling the body. Occurs in the absence of any causative skin, metabolic, or neurological disorders. Pathophysiology
The wheals, hypohidrosis, and pain seems to result from the low expression levels of acetylcholinesterase (AchE) and cholinergic receptor, muscarinic 3 (CHRM3) in the eccrine gland epithelial cells.