Neuropathy distal sensory peripheral

DSPN distal sensory peripheral neuropathy FED frontotemporal dementia... 

Distal sensory peripheral nenropathy (DSPN) has been associated with the nse of ddC, ddl, and stavndine, alone or in combination. The symptoms of this condition inclnde a bnming sensation in feet and hands, nnmbness and tingling in the feet, cramps in the legs, and absent ankle reflexes. The patient may also exhibit decreased sensation to temperatnre, pinprick, vibration, and proprioception (Dieterich, 2003). The symptoms are similar to HIV associated axonal neuropathy. This condition may become irreversible, so it is important to diagnose it earlier. The treatment of choice is symptomatic therapy and discontinuation of the toxic agent when possible. 

The women initially complained of numbness in their limbs, and subsequent nerve conduction studies showed alterations in peripheral nerve activity. The effect was diagnosed as primarily a distal sensory peripheral neuropathy. These cases were unusual because the effect was greater in the hands than in the feet, the reverse of most peripheral neuropathies. Sural nerve biopsies in two of the women performed 3-4 years after diagnosis revealed chronic neuropathy (axonopathy and myelinopathy) (Liss 1988). The authors did not establish a causal relationship with 1,1,1-trichloroethane. 

Diffuse infiltrative lymphocytosis syndrome AIDS Subacute Sjogren s-hke symmetric or asymmetric sensorimotor, painful, multiple mononeuritis or distal sensory neuropathy Angiocentric CDS hyperlymphocytosis in peripheral nerves vascular mural necrosis... 

A rabbit model of 2, 3 -dideoxycytidine neurotoxicity. Lab Invest 66(l) 63-74 Apostolski S, McAlarney T et al (1993) The gpl20 glycoprotein of human immunodeficiency virus type 1 binds to sensory ganghon neurons. Ann Neurol 34(6) 855-863 Araujo AP, Nascimento OJ et al (2000) Distal sensory polyneuropathy in a cohort of HIV-infected children over five years of age. Pediatrics 106(3) E35 Authier FJ, Gheradi RK (2003) Peripheral neuropathies in HIV-infected patients in the era of HAART. Brain Pathol 13(2) 223-228... 

Skopehtis EE, Kokotis PI et al (2006) Distal sensory polyneuropathy in HIV-positive patients in the HAART era an entity underestimated by clinical examination. Int J STD AIDS 17(7) 467-472 Smyth K, Affandi JS et al (2007) Prevalence of and risk factors for HIV-associated neuropathy in Melbourne, Australia 1993-2006. HIV Med 8(6) 367-373 Snider WD, Simpson DM et al (1983) Neurological complications of acquired immune deficiency syndrome analysis of 50 patients. Ann Neurol 14(4) 403-418 So YT, Olney RK (1994) Acute lumbosacral polyradiculopathy in acquired immunodeficiency syndrome experience in 23 patients. Ann Neurol 35(l) 53-58 So YT, Holtzman DM et al (1988) Peripheral neuropathy associated with acquired immunodeficiency syndrome. Prevalence and clinical features from a population-based survey. Arch Neurol 45(9) 945-948... 

Peripheral neuropathies maybe widely disseminated or focal. Patients with disseminated polyneuropathy, whether demyelinative or axonal, usually demonstrate distal sensory and/or motor impairment. Multifocal neuropathy, also referred to as mononeuropathy multiplex, is often a consequence of lesions affecting the vasa nervorum, the blood vessels that supply peripheral nerves. The most common diseases to compromise the vasa nervorum and cause infarction of nerve fascicles are diabetes mellitus and periarteritis nodosa. Other frequent causes of mononeuropathy multiplex include infection (e.g. Lyme disease and leprosy) and multiple compression injury (e.g. bilateral carpal tunnel syndrome). When mononeuropathy... 

The major dose-limiting toxicides of didanosine include peripheral neuropathy and pancreatitis. The neuropathy is typically symmetrical distal sensory neuropathy, which is reversible, and typically causes paresthesias, numbness and pain in lower extremities. Didanosine also causes retinal changes and optic neuritis. Other adverse effects include diarrhea, skin rash, headache, insomnia, seizures, hepatic toxicity, elevated hepatic transaminases and asymptomatic hyperuricemia. 

Beriberi (infantile and adult) and Wernicke s encephalopathy (WE) are clinical manifestations attributed to thiamine deficiency. Beriberi is characterized by peripheral neuropathy including sensory, motor, and reflex functions affecting the distal segments of limbs more severely than proximal ones (TanPhaichitr, 1985). WE is a metabolic disease due to thiamine deficiency and is characterized by lesions in the thalamus, hypothalamus (including mammillary nuclei), and cerebellum (Victor et al., 1971 Harper and Butterworth, 1997). 

A five-fold increase in the risk of distal sensory neuropathy has been reported in patients taking stavudine plus isoniazid (55 versus 11%) compared with patients taking stavudine without isoniazid (59). In nine of 12 patients, the neuropathy resolved on changing antiretroviral drugs. Peripheral neuropathy is a distressing complication during treatment with stavudine and the risk is considerably increased with co-administration of isoniazid. This combination of drugs should be avoided, if possible, in patients with tuberculosis and AIDS. 

Peripheral neuropathy may be the most frequent neurologic disorder associated with HIV infection (Cherry et al., 2005). Its symptoms cause substantial morbidity and discomfort to patients with AIDS. A 30%-35% prevalence of peripheral neuropathy has been documented in patients with HIV infection, but autopsy-based studies have found it in nearly 100% of patients who died of AIDS. The most common peripheral neuropathy associated with HIV occurs in the later stages of HIV disease, usually after the patient has had other AIDS defining illnesses. Symptoms of HIV-associated sensory neuropathies are almost identical to those of other sensory neuropathies. Both distal sensory neuropathy due to HIV infection (seen mainly in late disease) and antiretroxdral toxic neuropathy occur, or sensory neuropathy is caused by a combination of both (Cherry et al., 2005). 

In a peripheral neuropathy with sensory-nerve involvement (a) distally reduced pain sensation is tested by carefully testing distally to proximaUy up a limb with a disposable toothpick, but (b) to detect distal pain hypersensitivity, we carefully testproximally to distally down a limb. Hypersensitivity is produced by exces-... 

The earliest reports of neurological complications of AIDS described distal symmetrical, painful sensory neuropathy occurring in HIV patients (Snider et al. 1983). Dysimmune inflammatory polyneuropathy was subsequently recognized as a complication of AIDS (Lipkin et al. 1985). Progressive polyneuropathy associated with cytomegalovirus (CMV) infection was documented as the first truly opportunistic infection of the peripheral nerve (Eidelberg et al. 1986). 

Central nervous system effects predominate in acute exposures at massive doses, whereas peripheral neuropathy is more common with lower doses.After cessation of exposure to acrylamide, most cases recover, although the course of improvement can extend over months to years and depends on the severity of exposure. Because peripheral neurons can regenerate and central axons cannot, severely affected individuals may still experience residual ataxia, distal weakness, reflex loss, or sensory disturbance. 

Although MBK is considered to be only a mild sensory irritant with acute exposure, an outbreak of neuropathy among workers in a coated fabrics plant in 1973 revealed the more serious consequences of chronic exposure. Workers exposed to the mixed vapor of MBK (averaging 9.2 ppm in front of printing machines and 3 6 ppm behind) for 6-12 months with extensive skin exposure developed peripheral neuropathy. " The neurological pattern was one of a distal motor and sensory disorder, with minimal loss of tendon reflexes. In those with prominent motor involvement, initial... 

In combination with counts of ventral roots, femoral axon counts can be used to distinguish peripheral neuropathy from motor neuron death. The nerve has a primarily motor branch that innervates the quadriceps, and a primarily sensory branch that becomes the saphenous nerve more distally (Fig. 20.5). 

Peripheral neuropathy occurs in about 16% of patients with MGUS, being particularly common in those with an IgM monoclonal gammopathy [128], The IgM fraction of such patients includes antibodies to myelin-associated glycoprotein (MAG antibodies) that bind to determinants in peripheral nerve myelin, and, as shown by animal models, the antibodies mediate the myelin injury and secondary nerve damage [129]. The patients usually have a distal symmetric neuropathy, usually with predominant sensory affection, and the neurological symptoms frequently precede the detection of gammopathy [130]. 

CMT diseases are the most frequent hereditary sensory-motor neuropathies. They are distinguished from other types of genetic neuropathies, either purely motor, mainly distal and dysautonomous neuropathies which mainly alter sensory and sympathetic fibers of the peripheral nerves. We only deal here with CMT diseases and among the many genetic causes, those that give rise to primary demyelinating diseases of the peripheral nervous system (PNS). 

After initial contradictory reports it is now established that arsenic can cross the blood-brain barrier and produces alternations in whole rat brain biogenic amines levels in animals chronically exposed to arsenite (Tripathi et al, 1997). The neurological effects are many and varied. Usually, peripheral neuropathy, sensory neuropathy (Hafeman et al, 2005), and encephalopathy are the initial complaints associated with acute arsenic poisoning. Acute exposure to arsenic in humans has been shown to result in problems of memory, difficulties in concentration, mental confusion, and anxiety (Hall, 2002 Rodriguez et al, 2003). Other neurological symptoms arising due to arsenic are primarily those of a peripheral sensory neuritis, predominantly numbness, severe paresthesia of the distal portion of the extremities, diminished sense of touch, pain, heat and cold, and symmetrically reduced muscle power (Menkes, 1997). 

Leflunomide can cause a peripheral reversible neuropathy (49,62-65). This neuropathy is usually axonal in nature, affecting multiple sensory or motor nerves of distal extremities. The mean time of onset of peripheral neuropathy was 6 months after the start of leflunomide therapy, with a range of 3 days to 3 years. Neurological improvement was more likely after drug withdrawal within 30 days after the onset of the sjmptoms of neuropathy compared with continuous administration (63). 

Peripheral neuropathy presents as numbness, burning, and tingling in a glove-and-stocking distribution. Symptoms usually begin 24-72 hours after treatment with paclitaxel, with a symmetrical distal loss of sensation. Most cases occur at doses over 200 mg/m and particularly after multiple courses (24—26). Mild to moderate sensory neuropathy has occurred in 52% of patients treated with doses of 175 mg/m, while only 36% experienced neuropathy at doses of at least 135 mg/m (17,24,28,29). At the lower dose of 135 mg/m, the effects are usually limited to a mild sensory neuropathy (17,29). 

Nervous system About 30% of patients treated with docetaxel develop symptoms of peripheral neuropathy [112 ]. Generally, the symptoms settle within months. Peripheral neuropathy is less frequent with docetaxel than with paclitaxel grade 3/4 sensory neuropathy occurs in about 5% of patients treated with docetaxel 100 mg/m [126 ]. Proximal and distal muscle weakness has also been reported (about 5% in a review of 186 patients in phase I and phase II studies) [127 ]. The pathogenesis, incidence, susceptibility factors, diagnosis, characteristics, and management of taxane-induced peripheral neuropathy have been critically reviewed [128 ]. 

Drug overdose An acute peripheral neuropathy with quadriparesis, lancinating pain, sensory loss, paresthesia of the distal limbs, and a vocal fold palsy occurred 1 month after a disulfiram overdose of 130 tablets in a 49-year-old woman [51 ]. A severe toxic encephalopathy with coma, convulsions, and quadriparesis occurred in a 35-year-old man who took an overdose of disulfiram [52 ]. 

Charcot-Marie-Tooth disease is a complex and heterogeneous group of inherited disorders of the peripheral nervous system, also known as hereditary motor and sensory neuropathies, that is characterized by hypertrophied peripheral neuropathy due to the abnormal growth (like an onion bulb) of Schwann cells (Fig. 4.6a,b). The most common clinical features include unsteady gait due progressive distal weakness of peroneal muscles, pes cavus, depressed or absent deep tendon reflexes, and mild sensory loss. The histopathologic abnormalities involve all nerves in the body and occur predominantly in the fascicles. Although the classification system of Charcot-Marie-Tooth disease is... 

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