Neurological manifestations of HIV infection

Neurological manifestations of HIV infection This article only deals with the consequences of HIV infection on the central and peripheral nervous system.
Neurological manifestations of HIV infection in the central nervous system
Primary HIV infection may be associated with aseptic meningitis and acute encephalopathy with opportunistic infections or organ systemic infection that follows HIV-induced immunodeficiency. Among the most important central nervous system complications in HIV infection include cerebral toxoplasmosis, primary central nervous system lymphoma, progressive multifocal leucoencefalita. Aseptic meningitis associated with HIV is characterized by fever, headache, meningeal signs and sometimes cranial nerve palsies V, VII and VIII. Analysis of cerebrospinal fluid is observed Pleocytosis mononuclear proteinorahie glicorahie high and normal. HIV diagnosis of aseptic meningitis is established by documenting anti-HIV seroconversion and intrathecal synthesis of anti-HIV antibodies. Progression of HIV infection but is associated with an increased incidence of encephalopathy and dementia. Dementia in this infection is known as the AIDS dementia complex or complex motor / cognitive associated with HIV. Clinically, these patients suffer from a lack of concentration, memory loss, slowness in thinking, apathy, depression, social withdrawal and personality changes. Half of the patients are common signs or symptoms of motor dysfunction as leg paralysis, difficulty with balance, ataxia, tremor and signs of pyramidal pathway. Neurons may be affected by the release of cytokines, neurotoxins and other soluble factors from infected immune cells, macrophages or glial cells. Unfortunately, the average survival in severe dementia rarely exceed six months from the onset of symptoms. One quarter of patients are found in laboratory tests and cerebrospinal fluid lymphocytic Pleocytosis proteinorahie increased. CT and MRI (magnetic resonance imaging) show a diffuse cerebral atrophy and an enlargement of the ventricles. Neuropathological markers of encephalitis caused by HIV are represented by the presence of multinucleated giant cells present both in the cortex, and the white matter. These giant cells containing HIV particles. There is no definitive treatment for dementia associated with HIV. Treatment is symptomatic and includes administration of zidovudine and didanosine. It was found that patients receiving higher doses of zidovudine (1000 mg / day) have a better evolution than those who receive usual doses.
Peripheral neurological manifestations of HIV infection
Even in the early stages of HIV infection, may develop distal sensory and motor polyneuropathy. More commonly affected limbs. This event is characterized by pain in the legs and / or superior character that exacerbates the burning or tingling at night. The pain is accompanied by numbness and limb. When the legs are affected, pain and numbness in the plant initially localize (feet) and leg, then during the climb to the thighs and eventually affects the hips and lumbar region. In general symptoms are symmetrical. Pain can have a very lively character, which can immobilize the patient in bed. Sometimes a touch of sore feet exacerbate crises. The patient generally does not support articles of clothing or sheet covering her legs because of unbearable pain.
Neurological examination revealed tenderness of the legs reduced vibration, lower temperature and lower limb bone-tendon reflexes diminished or abolished (achilian and rotulian reflex). Paralysis or atrophy as motor changes are mild in comparison with sensory symptoms and signs. If paralysis occurs, it is limited to intrinsic foot muscles. Trophic changes are present and skin atrophy, loss of hair on legs, abnormal nail growth, swelling and vasomotor disturbances. Muscle strength is generally not affected. In advanced stages of HIV infection, some patients may develop an autonomous neuropathy is manifested by diarrhea, cardiac arrhythmias and orthostatic hypotension.
Immunosuppressive drugs may worsen sensory-motor polyneuropathy by increasing the body's viral load. Laboratory examinations objectifies decrease nerve conduction velocity and electromyography showed axonal neuropathy both in small fibers and the large ones. Sensory-motor polyneuropathy may also result from alcohol toxicity, vitamin B12, thiamine, pyridoxine. Other causes are diabetes mellitus and some antiviral drugs (didanosine, stavudine, zalcitabine or dideoxicidina) whose adverse effects translate into exacerbation polyneuropathy. It is very important to differentiate between HIV infection and other causes that may lead to sensory-motor polyneuropathy.
Many patients are in advanced stages of HIV infection with the virus develop poliradiculopatie citomegaliei. Pathologist, it begins with damage poliradiculopatie lumbosacral roots and clinical patients experience pain and loss of sensation in the feet and legs. Some of these patients have associated signs and symptoms of myelitis. In a finding of cerebrospinal fluid polymorphonuclear Pleocytosis and through polymerization reaction can detect the virus DNA citomegaliei. Patients experiencing citomegaliei virus infection should be treated with ganciclovir or foscarnet. For pain therapy can be successfully used analgesics, tricyclic antidepressants, anticonvulsants and capsaicin ointment. To remove postural hypotension that fludrocortizonul mineralocorticoid is administered.
At a quarter of HIV infected patients develop a chronic progressive myelopathy that affects the posterior and lateral horns of the spinal cord. Clinically, in these patients is a paraparesis spastic ataxia objectifies sensibitatii reduce vibration and positional and urinary incontinence. Most patients experience associated encephalopathy or dementia and HIV. Pathologically, there is a vacuolar degeneration of white matter in the posterior and lateral horns, resulting in severe swelling of the myelin sheath of nerve fibers. You can see the lymph nodes of lumbar spinal nerve roots and sacred, these events appear in the beam gracilis secondary degeneration of the posterior horns. Myelopathy treatment is oral zidovudine and didanosine not bring much improvement.
Other patients may develop during HIV infection and myopathy, a condition that is not tied to a particular stage of HIV infection, it can appear at any stage. Clinically, the myopathy is characterized by proximal muscle paralysis and muscle. Laboratory analysis reveals that aldoloaza elevated muscle enzyme, creatine kinase, lactic dehydrogenase. Muscle biopsy is sometimes necessary for treatment, a biopsy relevad miofibrilelor inflammation or degeneration and necrosis.
Myopathy may occur as adverse drug reaction zidovudine therapy used in HIV infection. Usually, this effect occurs at 6 months after treatment and is accompanied by pain more intense than on HIV myopathy and serum enzyme concentrations are increased. Muscle biopsy is required for differentiation of HIV myopathy, observing microscopic examination is more pronounced necrosis of muscle fibers and a lower inflammatory reaction. Most effective treatment is discontinuation of medication with zidovudine that leads to the disappearance of symptoms. If it is not necessarily required further administration of zidovudine, corticosteroids may be associated to it which also reduce the adverse effects of zidovudine.