1. Chronic inflammatory demyelinating polyneuropathy (CIDP) This polyneuropathy develops over weeks or months, usually with a persistent but relapsing and remitting course. CSF protein is raised and, usually, segmental demyelination is seen in peripheral nerves. CIDP responds to steroids (long term, low dose) and to i.v. immunoglobulin (for exacerbations).

2. Diphtheritic neuropathy Palatal weakness followed by pupillary paralysis and a sensorimotor neuropathy occur several weeks after the throat infection. Diphtheritic neuropathy Palatal weakness followed by pupillary paralysis and a sensorimotor neuropathy occur several weeks after the throat infection. Idiopathic chronic sensorimotor neuropathy The patient complains of progressive symmetrical numbness and tingling in hands and feet, spreading proximally in glove and stocking distribution. There is distal weakness which also ascends. Rarely cranial nerves are affected. Tendon reflexes become absent. Symptoms may progress over many months, remain static or occasionally remit. Autonomic features are sometimes seen. Idiopathic chronic sensorimotor neuropathy The patient complains of progressive symmetrical numbness and tingling in hands and feet, spreading proximally in glove and stocking distribution. There is distal weakness which also ascends. Rarely cranial nerves are affected. Tendon reflexes become absent. Symptoms may progress over many months, remain static or occasionally remit. Autonomic features are sometimes seen.

3. Toxic, metabolic and vitamin- deficiency neuropathies Metabolic neuropathies Diabetes mellitus Several varieties of neuropathy occur in diabetes: Metabolic neuropathies Diabetes mellitus Several varieties of neuropathy occur in diabetes: symmetrical sensory polyneuropathy symmetrical sensory polyneuropathy acute painful neuropathy acute painful neuropathy mononeuropathy and multiple mononeuropathy: mononeuropathy and multiple mononeuropathy: cranial nerve lesionscranial nerve lesions isolated peripheral nerve lesions (e.g. median)isolated peripheral nerve lesions (e.g. median) diabetic amyotrophy diabetic amyotrophy autonomic neuropathy. autonomic neuropathy.

4. Uraemia Uraemia Progressive sensorimotor neuropathy develops in chronic uraemia. The response to dialysis is variable but the neuropathy usually improves after renal transplantation. Progressive sensorimotor neuropathy develops in chronic uraemia. The response to dialysis is variable but the neuropathy usually improves after renal transplantation. Thyroid disease A mild chronic sensorimotor neuropathy is sometimes seen in both hyperthyroidism and hypothyroidism Myopathy also occurs in hyperthyroidism Thyroid disease A mild chronic sensorimotor neuropathy is sometimes seen in both hyperthyroidism and hypothyroidism Myopathy also occurs in hyperthyroidism

5. Refsum's disease This is a rare condition inherited as an autosomal recessive. There is a sensorimotor polyneuropathy with ataxia, retinal damage and deafness. It is due to defective phytanic acid metabolism Refsum's disease This is a rare condition inherited as an autosomal recessive. There is a sensorimotor polyneuropathy with ataxia, retinal damage and deafness. It is due to defective phytanic acid metabolism

6. Alcohol Alcohol Polyneuropathy, mainly in the lower limbs, occurs with chronic excess alcohol. Calf pain is common. Thiamine is the treatment, but the response is variable, even with complete abstention. Recurrence (and progression) occurs with even small amounts of alcohol. Polyneuropathy, mainly in the lower limbs, occurs with chronic excess alcohol. Calf pain is common. Thiamine is the treatment, but the response is variable, even with complete abstention. Recurrence (and progression) occurs with even small amounts of alcohol. Drugs and industrial toxins Many drugs) and a wide variety of industrial toxins cause polyneuropathy. Drugs and industrial toxins Many drugs) and a wide variety of industrial toxins cause polyneuropathy. Toxins include: Toxins include: lead poisoning - motor neuropathy lead poisoning - motor neuropathy acrylamide (plastics industry), trichlorethylene, hexane and other fat-soluble hydrocarbons (e.g. glue-sniffing,) - progressive sensorimotor polyneuropathy acrylamide (plastics industry), trichlorethylene, hexane and other fat-soluble hydrocarbons (e.g. glue-sniffing,) - progressive sensorimotor polyneuropathy arsenic and thallium - polyneuropathy, initially sensory arsenic and thallium - polyneuropathy, initially sensory

7. Phenytoin M Phenytoin M Chloramphenicol S, M Chloramphenicol S, M Metronidazole S, S/M Metronidazole S, S/M IsoniazidS, S/M IsoniazidS, S/M Dapsone M Dapsone M Anti-retroviral drugs S > M Anti-retroviral drugs S > M NitrofurantoinS/M NitrofurantoinS/M VincristineS > M VincristineS > M PaclitaxelS > M PaclitaxelS > M

8. Vitamin-deficiency neuropathies Vitamin deficiencies cause nervous system diseases that are largely preventable and potentially reversible if treated early - and inexorably progressive if not. Deficiencies (often of multiple vitamins) occur in malnutrition Vitamin-deficiency neuropathies Vitamin deficiencies cause nervous system diseases that are largely preventable and potentially reversible if treated early - and inexorably progressive if not. Deficiencies (often of multiple vitamins) occur in malnutrition

9. Vitamin B12 (cobalamin) Deficiency causes damage to the spinal cord, peripheral nerves and brain. Subacute combined degeneration of the cord (SACD). Combined spinal cord and peripheral nerve damage is a sequel of Addisonian pernicious anaemia and rarely other causes of vitamin B12 deficiency Vitamin B12 (cobalamin) Deficiency causes damage to the spinal cord, peripheral nerves and brain. Subacute combined degeneration of the cord (SACD). Combined spinal cord and peripheral nerve damage is a sequel of Addisonian pernicious anaemia and rarely other causes of vitamin B12 deficiency The patient complains initially of numbness and tingling of fingers and toes. There is combined distal sensory loss, particularly posterior column, absent ankle jerks (neuropathy), with cord disease - exaggerated knee jerks, extensor plantar responses. Optic atrophy and retinal haemorrhage may occur. In later stages sphincter disturbance, severe generalized weakness and dementia develop. Exceptionally, dementia develops in the early stages. Without treatment, SACD is fatal within 5 years. Macrocytosis with megaloblastic bone marrow are usual though n The patient complains initially of numbness and tingling of fingers and toes. There is combined distal sensory loss, particularly posterior column, absent ankle jerks (neuropathy), with cord disease - exaggerated knee jerks, extensor plantar responses. Optic atrophy and retinal haemorrhage may occur. In later stages sphincter disturbance, severe generalized weakness and dementia develop. Exceptionally, dementia develops in the early stages. Without treatment, SACD is fatal within 5 years. Macrocytosis with megaloblastic bone marrow are usual though n

10. Charcot-Marie-Tooth disease) Charcot-Marie- Tooth (CMT) disease is also called peroneal muscular atrophy. CMT describes the common clinical phenotype - distal limb wasting and weakness that slowly progresses over many years, mostly in the legs, with variable loss of sensation and reflexes. In advanced disease, distal wasting is so marked that the legs are said to resemble inverted champagne bottles. Mild cases have pes cavus and clawing of the toes that can pass unnoticed. Multiple genetic variants of the CMT phenotype are now recognized, Charcot-Marie-Tooth disease) Charcot-Marie- Tooth (CMT) disease is also called peroneal muscular atrophy. CMT describes the common clinical phenotype - distal limb wasting and weakness that slowly progresses over many years, mostly in the legs, with variable loss of sensation and reflexes. In advanced disease, distal wasting is so marked that the legs are said to resemble inverted champagne bottles. Mild cases have pes cavus and clawing of the toes that can pass unnoticed. Multiple genetic variants of the CMT phenotype are now recognized,

11. Neuropathy in cancer Polyneuropathy is seen as a non-metastatic manifestation of malignancy, sometimes with anti-Hu antibodies. Polyneuropathy occurs in myeloma and other dysproteinaemic states, probably owing to impaired perfusion of nerve trunks or to demyelination associated with allergic reactions affecting peripheral nerves. Individual nerves are sometimes infiltrated with malignant cells Neuropathy in cancer Polyneuropathy is seen as a non-metastatic manifestation of malignancy, sometimes with anti-Hu antibodies. Polyneuropathy occurs in myeloma and other dysproteinaemic states, probably owing to impaired perfusion of nerve trunks or to demyelination associated with allergic reactions affecting peripheral nerves. Individual nerves are sometimes infiltrated with malignant cells

12. Autonomic neuropathy Autonomic neuropathy causes postural hypotension, urinary retention, impotence, diarrhoea (or occasionally constipation), diminished sweating, impaired pupillary responses and cardiac arrhythmias. This develops in diabetes mellitus, in amyloidosis and may complicate Guillain-Barré syndrome. Many varieties of neuropathy cause autonomic failure in a mild, and often subclinical, form. Occasionally, when there is damage to small myelinated and non-myelinated B and C fibres, clinical features of the autonomic neuropathy predominate, e.g. in diabetes. Autonomic neuropathy causes postural hypotension, urinary retention, impotence, diarrhoea (or occasionally constipation), diminished sweating, impaired pupillary responses and cardiac arrhythmias. This develops in diabetes mellitus, in amyloidosis and may complicate Guillain-Barré syndrome. Many varieties of neuropathy cause autonomic failure in a mild, and often subclinical, form. Occasionally, when there is damage to small myelinated and non-myelinated B and C fibres, clinical features of the autonomic neuropathy predominate, e.g. in diabetes.

13. PLEXUS AND NERVE ROOT LESIONS THORACIC OUTLET SYNDROME THORACIC OUTLET SYNDROME A fibrous band or cervical rib extending from the tip of the C7 transverse process to the first rib stretches across the lower brachial plexus (roots C8 and T1). There is forearm pain (ulnar border), T1 sensory loss and thenar muscle wasting, principally abductor pollicis brevis. Horner's syndrome may develop. The rib or band can be excised. In some patients the rib or band causes subclavian artery or venous occlusion. Neurological and vascular problems rarely occur together. Thoracic outlet syndrome is also used to describe ill-defined upper limb symptoms - usually on poor evidence. A fibrous band or cervical rib extending from the tip of the C7 transverse process to the first rib stretches across the lower brachial plexus (roots C8 and T1). There is forearm pain (ulnar border), T1 sensory loss and thenar muscle wasting, principally abductor pollicis brevis. Horner's syndrome may develop. The rib or band can be excised. In some patients the rib or band causes subclavian artery or venous occlusion. Neurological and vascular problems rarely occur together. Thoracic outlet syndrome is also used to describe ill-defined upper limb symptoms - usually on poor evidence.

14. Malignant infiltration Metastatic disease of nerve roots of the brachial or lumbosacral plexus causes a painful radiculopathy. A common example is an apical bronchial neoplasm (Pancoast's tumour) causing a T1 and sympathetic outflow lesion. There is wasting of small hand muscles, pain, T1 sensory loss with ipsilateral Horner's syndrome. This also occurs in apical TB. Metastatic disease of nerve roots of the brachial or lumbosacral plexus causes a painful radiculopathy. A common example is an apical bronchial neoplasm (Pancoast's tumour) causing a T1 and sympathetic outflow lesion. There is wasting of small hand muscles, pain, T1 sensory loss with ipsilateral Horner's syndrome. This also occurs in apical TB.