Aetiology
Paraesthesias may be due to conditions that affect sensory function at the level of the peripheral nerve or, less commonly, at the level of the dorsal root ganglion, dorsal sensory nerve roots, spinal cord, or brain. The underlying conditions may be inherited or acquired. A knowledge of the anatomy of the somatosensory pathways is required to understand the patterns of paraesthesia produced by different processes.
Causes include:
Nerve compression or injury
Nerve demyelination and/or axonal degeneration
Endocrine of metabolic disease
Nutritional deficiency
Drug or toxin exposure
Macrovascular disease
Infection
Psychogenic disorders
Vasculitic or inflammatory disease
Genetic disorders
Other (e.g., focal seizures; paraneoplastic sensory neuropathy)
[Figure caption and citation for the preceding image starts]: Ascending sensory pathways of the spinal cord. The dorsal column system and spinothalamic tract are the major ascending pathways that connect the periphery with the brain.Betts JG, Young KA, Wise JA et al.Anatomy and physiology. Houston, TX:OpenStax; 2013 (CC BY4.0 - https://creativecommons.org/licenses/by/4.0/) [Citation ends].
Nerve compression or injury
Focal nerve entrapment syndromes can lead to paraesthesias in the distribution of the involved peripheral nerve if sensory nerve fibres are involved. Sensory symptoms usually appear first, followed by motor weakness in the distribution of the affected nerve. Symptoms typically follow the pattern of the distribution of the nerve distal to the site of compression or entrapment. Common entrapment neuropathies include:
Median neuropathy at the wrist (carpal tunnel syndrome)
Ulnar neuropathy at the elbow (cubital tunnel syndrome)
Fibular (peroneal) neuropathy at the knee
Neuropathy of the lateral femoral cutaneous nerve of the thigh (meralgia paraesthetica)
Trigeminal neuropathy or neuralgia due to micro-vascular compression at the entry zone of the nerve into the pons.
Rarer entrapment neuropathies include tibial neuropathy at the ankle (tarsal tunnel syndrome) and cutaneous sensory neuropathy of the dorsal branches of the spinal nerves in selected dermatomes (T2-T6) unilaterally on the upper back (notalgia paraesthetica).
Vascular or mass lesions of various types can lead to peripheral nerve compression or entrapment and present with paraesthesias.[1][2][3][4][5]
Entrapment syndromes involving the brachial or lumbosacral plexus can be produced by traumatic injury to the plexus, or by vascular abnormalities (e.g., haemangioma), or by direct carcinomatous invasion of the plexus by a metastatic tumour or lymphoma.[6]
Entrapment syndromes involving the dorsal spinal nerve roots are divided into cervical, thoracic, and lumbosacral radiculopathies, depending on the nerve root affected, and can be produced by spondylosis, stenosis, intervertebral disc herniation, degenerative arthritis, or mass compression.[7][8][9][10] Spinal cord compression syndromes can occur as a result of spine trauma such as vertebral compression fractures, intervertebral disc herniation, primary or metastatic spinal tumour, vascular malformations or infection.[8][11]
Nerve demyelination and/or axonal degeneration
Multiple sclerosis
A relapsing and remitting focal inflammatory disorder of the central nervous system (CNS), clinically defined by two episodes of neurological dysfunction separated in space and time. Lesions can affect the brain, spinal cord, or optic nerves. Lesions that affect the somatosensory pathway in the spinal cord, brainstem, or somatosensory cortex can produce paraesthesias. Rarely, a patient may present with numb chin syndrome as an early manifestation of multiple sclerosis, where there are unilateral chin paraesthesias.[12]
Neuromyelitis optica spectrum disorder (NMOSD or Devic's disease)
Auto-antibodies (NMO-IgG) disrupt key ion channels on the surface of astrocytes in the CNS that ultimately leads to optic nerve (loss of vision) and spinal cord dysfunction (paraesthesias, weakness, and bowel and bladder dysfunction).
Acute disseminated encephalomyelitis
An acute monophasic inflammatory disorder of the CNS, pathologically similar to multiple sclerosis, which produces encephalitis with constitutional symptoms. Frequently triggered by an antecedent infection or vaccination.
Acute inflammatory demyelinating polyradiculoneuropathy (AIDP)
The most commonly encountered variant of Guillain-Barré syndrome. A demyelinating polyneuropathy characterised by an immune-mediated attack on the myelin sheath or Schwann cells of sensory and motor nerves. The characteristic clinical presentation is of a progressive symmetric muscle weakness affecting lower extremities before upper extremities, and proximal muscles before distal muscles, accompanied by paraesthesias in the feet and hands.
Chronic inflammatory demyelinating polyradiculoneuropathy (CIDP)
An acquired, demyelinating, peripheral neuropathy of presumed autoimmune aetiology. The course is usually either chronic progressive (over the course of 8 weeks or more) or relapsing and remitting. The clinical phenotype consists of proximal and distal symmetric weakness, distal sensory loss, and absent reflexes.
Chronic inflammatory demyelinating sensory polyradiculopathy
An acquired demyelinating condition that preferentially affects large myelinated fibres of the posterior roots. Presents with gait ataxia, large-fibre sensory loss, and paraesthesias.
Anti-myelin-associated glycoproteins (MAG) peripheral neuropathy
Rare CIDP-like condition affecting mainly middle-aged men where auto-antibodies against MAG cause paraesthesias (hands and feet), tremor, and ataxia.
Distal symmetric polyneuropathy
A length-dependent or distally predominant peripheral neuropathy, which is symmetric in distribution, and may involve pure sensory or mixed sensory and motor nerves. It may involve primarily small unmyelinated sensory nerve fibres exclusively, but more commonly involves both large and small sensory and motor nerve fibres. It may occur as a consequence of a variety of acquired causes, including infectious, inflammatory, toxic, endocrine, metabolic, and nutritional conditions. It is the most common clinical manifestation of peripheral nerve disease, the classic 'stocking and glove' distribution of sensory and motor symptoms and findings. It may be due to demyelination, axonal degeneration, or a combination of both pathological processes affecting the peripheral nerves.[13][14]
Endocrine or metabolic disease
Diabetes mellitus
Hyperglycaemia initiates a process of nerve damage affecting peripheral nerve fibres and Schwann cells. The pathophysiology is complex and includes oxidative and nitrosative stress, redox imbalance, endothelial dysfunction, perturbations in prostaglandin metabolism, and direct hypoxia and ischaemia of nerve trunks and ganglia. These changes impair mitochondrial function and neurotrophic support. Ongoing hyperglycaemia produces progressive damage and loss of peripheral nerve fibres and impaired sensory function.
Hypertriglyceridaemia
High triglyceride levels are associated with a predominantly sensory axonal length dependent polyneuropathy that often presents with burning paraesthesias in the feet. The cause is unknown.
Uraemia
A clinical syndrome of metabolic abnormalities and fluid, electrolyte, and hormone imbalance that develops in the context of deteriorating renal function. Patients develop a generalised peripheral neuropathy mediated by toxic substances that accumulate in the blood, and may also develop focal nerve entrapment syndromes such as carpal tunnel syndrome or median nerve neuropathy. Uraemic encephalopathy may also occur.
Hypocalcaemia
Calcium plays a crucial role in neural function, and hypocalcaemia produces a range of neurological signs and symptoms including paraesthesias affecting the fingertips, toes, and perioral region.
Hypothyroidism
Produces a peripheral neuropathy with paraesthesias, but the mechanism is not understood. Hypothyroidism can also produce specific entrapment neuropathies of which median nerve neuropathy is the most common.
Nutritional deficiency
Vitamin B12 deficiency[15][16]
Vitamin B12 is critical in the production of S-adenosylmethionine, which is thought to be important in neural function. It is also an essential co-factor in haematopoiesis. Vitamin B12 deficiency usually manifests as a macrocytic anaemia with or without paraesthesias, but paraesthesias may be the only presenting feature in some cases.
Subacute combined degeneration of the cord is a severe complication of vitamin B12 deficiency.
Vitamin B6 deficiency or excess[16]
Vitamin B6 is an important co-factor in amino acid and glycogen metabolism. Neurological symptoms are wide ranging and include distal limb numbness, paraesthesias, and weakness with impaired vibration and proprioception and sensory ataxia. Other signs include seborrhoeic dermatitis, atrophic glossitis with ulceration, and angular cheilitis.
Vitamin B1 deficiency[16]
Thiamine is an important co-factor in carbohydrate metabolism. Deficiency produces symptoms of resting tachycardia, weakness, and decreased deep tendon reflexes. Some patients develop a peripheral neuropathy. Patients also have associated cardiac abnormalities and vocal cord paralysis.
Vitamin E deficiency[16]
Vitamin E is an important lipid-soluble antioxidant nutrient. Deficiency produces nerve damage. Peripheral neuropathy is a late manifestation, with spinocerebellar ataxia and visual changes occurring earlier.
Copper deficiency[17]
Copper deficiency produces anaemia and neurodegeneration, which manifests with progressive spasticity, ataxia, and a peripheral sensory neuropathy. Causes include copper-deficient total parenteral nutrition, gastric bypass surgery, and zinc toxicity.
Drug or toxin exposure
Alcohol
Chronic high alcohol intake produces a peripheral polyneuropathy, although the aetiology is unclear. The neuropathy is partly related to the direct toxic effects of alcohol and partly due to associated vitamin and mineral deficiencies. Sensory symptoms predominate, but motor, proprioceptive, and autonomic manifestations also occur.
The polyneuropathy is known as dying-back neuropathy. Symptoms start distally. Initially, patients develop numbness of the soles, followed by paraesthesias of feet and legs, especially at night. Paraesthesias slowly progress proximally, and become painful (described as burning or lancinating). Paraesthesias of the fingers and hands often appear once symptoms extend above the ankle level. Motor signs include weakness and muscle wasting.
Patients may also develop loss of proprioception (giving rise to abnormal gait independent of cerebellar problems) and, rarely, autonomic dysfunction.
Drug-induced
Common causes of peripheral neuropathy include chemotherapy agents (cisplatin, vincristine, cytosine arabinoside, thalidomide, paclitaxel), antibiotics (metronidazole, nitrofurantoin), antiretroviral agents (zidovudine, stavudine, lamivudine), and antiepileptics (phenytoin).[18] Paraesthesia is one of the most commonly reported adverse drug reactions of topiramate, a drug used to treat a number of neuropsychiatric conditions including alcohol dependence, essential tremor, binge-eating disorder, bulimia nervosa, migraine, and epilepsy.[19]
Heavy metals
Lead, arsenic, mercury, and thallium can cause a peripheral sensory polyneuropathy. Toxicity can result from a range of occupational, environmental, or recreational exposures. Thallium exposure may also occur through contamination of cocaine, heroin, and herbal products. There is increasing concern about mercury exposure from contaminated fish.[20]
Hexane
Hexane, from glue-sniffing behaviour or industrial exposure, can produce neurotoxicity that is attributed to 2,5-hexanedione formed from the parent compound. Patients develop a dying-back neuropathy similar to that produced by alcohol.
Ingested neurotoxins
Ciguatera toxin is an odourless and tasteless toxin found in reef fish, most commonly barracuda, grouper, red snapper, eel, amberjack, sea bass, and Spanish mackerel. The toxin is not destroyed by cooking. Eating ciguatera-contaminated fish results in poisoning. Symptoms begin 6 to 8 hours after ingestion and include paraesthesias, abdominal pain, nausea, vomiting, diarrhoea, dizziness, and vertigo.
Saxitoxin, one of the most potent natural toxins, is produced by some species of marine dinoflagellates and cyanobacteria and accumulates in shellfish. The toxin acts on voltage-gated sodium channels and prevents nerve conduction. Ingestion of contaminated shellfish produces paralytic shellfish poisoning. Symptoms begin within 30 minutes of ingestion and include paraesthesias of the lips, tongue, and gums, which then rapidly progress to involve the extremities. Headaches, ataxia, and motor and cranial nerve abnormalities may also occur.
Radiation
Post radiation-induced brachial plexopathy or lumbosacral plexopathy may occur if the nerves are in the field of external beam radiation. Symptoms may manifest years after the initial radiation exposure. In addition, late effects of radiation to the pelvis may include a cauda equina syndrome or lumbosacral polyradiculopathy.[21]
Macrovascular disease
Stroke or transient ischaemic attack
An ischaemic or haemorrhagic stroke in the somatosensory cortex may cause paraesthesias and loss of sensation in the face or extremities. If the stroke affects the brainstem, patients may also have symptoms of weakness, as the motor and sensory pathways in the brainstem are in close proximity. An isolated infarct of the splenium (posterior portion of the corpus callosum) has been found to rarely cause hemibody paraesthesias as the only manifestation.[22]
Migraine
Some migraine headaches are associated with an aura that includes focal or unilateral neurological symptoms. These may include paraesthesias on the face or the extremities, as part of the headache or as a complication of medication (e.g., those containing ergot derivatives used to treat the migraine).[23][24]
Peripheral vascular disease
Paraesthesia is one of the classic signs of limb ischaemia, along with pain, pallor, cold, absent pulses, and paralysis. The paraesthesia is usually in a 'glove and stocking' distribution.
Other cerebrovascular disease
Unilateral paraesthesias may rarely be associated with other vascular abnormalities in the brain and spinal cord, including cavernous malformations and intravascular lymphoma.[8][25] Cavernous malformations most often occur in the brain but can also rarely affect extra-cranial areas such as the spinal cord, leading to paraesthesias in the extremities.[8] Intravascular large B-cell lymphoma is a rare form of diffuse large B-cell lymphoma that presents with CNS involvement in 75% to 85% of patients.[25] Neurological symptoms include sensory and motor neuropathies, paraesthesia, muscle weakness, hemiparesis, meningoradiculitis, dysarthria, aphasia, seizures, transient visual loss, vertigo, and impaired cognitive function.[25]
Infection
HIV
HIV produces a peripheral neuropathy that may be due partly to direct infection of dorsal root ganglia and partly to neurotoxic cytokines secreted by locally invading macrophages. Neuropathy may also be produced by associated infections. Cytomegalovirus can produce a polyradiculopathy in immunosuppressed patients, especially those with AIDS.
Human T-lymphotropic virus (HTLV)
HTLV is a retrovirus that can cause a progressive myelopathy (tropical spastic paraparesis) resulting in leg weakness, back pain, paraesthesias, and bowel and bladder dysfunction. It has also been implicated as a cause of sensory polyneuropathies.
Leprosy
A chronic infectious disease caused by Mycobacterium leprae that affects the skin and peripheral nerves, producing characteristic skin lesions with sensory and/or motor deficits.
Lyme disease (Borrelia burgdorferi)
Lyme disease is a zoonotic infection caused by a spirochete of the genus Borrelia, which is transmitted to humans by ticks. Radiculopathy is a complication of the disease. Peripheral neuropathy is a late complication of CNS involvement.
Herpes zoster infection (shingles)
A viral infection that disseminates through regional lymph nodes to the liver, spleen, and other cells within the reticuloendothelial system. Symptoms appear when the infection spreads from the reticuloendothelial system to the skin and mucous membranes. Initial symptoms are pain and paraesthesia. These are shortly followed by a characteristic rash in the affected dermatome.
Herpes simplex infection
Causes oral, genital, and ocular ulcers. Patients report a localised paraesthesia that forms part of the prodrome prior to the onset of the ulcers. The paraesthesia may be the only symptom in some patients.
Neurosyphilis
A sexually transmitted infection caused by Treponema pallidum. Associated with primary (local), secondary (disseminated), and tertiary (end-organ complications including neurosyphilis) infection. Neurosyphilis can produce a polyradiculopathy that usually affects the lower limbs. It can also produce damage to the dorsal column of the spinal cord, producing a syndrome called tabes dorsalis. Key features of tabes dorsalis include Argyll-Robertson pupils, ataxia, loss of deep tendon reflexes, and loss of proprioception, vibration, and position sense.
Psychogenic disorders
Panic attacks with hyperventilation
Patients may report perioral and distal extremity paraesthesias that are associated with anxiety or panic symptoms and hyperventilation. An extremely common cause of paraesthesias.
Conversion and somatic symptom disorders
Caused by an underlying psychiatric condition. The distribution of the paraesthesias may be focal or hemifacial or hemibody, but does not correlate with a pathological lesion or abnormality of the underlying sensory pathway.
Vasculitic or inflammatory disease
Vasculitic conditions can produce either mononeuritis multiplex (a condition of progressive motor and sensory deficits in the distribution of specific peripheral nerves) or a polyneuropathy. Vasculitic neuropathies are often painful.[26] Peripheral sensory neuropathy may also occur due to direct immune-mediated nerve inflammation caused by auto-antibodies or a reaction to monoclonal protein deposition. In some cases, a combination of these aetiologies is present. Causes include:
Vasculitis associated with connective-tissue diseases such as systemic lupus erythematosus (SLE) and rheumatoid arthritis. SLE is associated with a distal symmetric sensory neuropathy with progressive distal lower extremity paraesthesias, which may progress to involve motor nerve fibres[27]
Polyarteritis nodosa, a vasculitic condition that affects only medium-sized blood vessels. Associated abnormalities include arthritis, purpura or other skin manifestations, abdominal pain due to abdominal organ ischaemia, and renal failure[28]
Churg-Strauss syndrome, a vasculitic condition that affects small- and medium-sized blood vessels. Associated abnormalities include asthma, eosinophilia, and abnormal infiltrates on chest x-ray[26][29][30][31]
Granulomatosis with polyangiitis (formerly known as Wegener's granulomatosis), a vasculitis affecting small- and medium-sized blood vessels with lesions of the nasal passages, lungs, and kidneys[32][33][34]
Microscopic polyangiitis, a vasculitic condition that affects small vessels. Associated abnormalities include palpable purpura or other skin manifestations, pulmonary rales, hypertension, heart failure, and renal failure
Sjogren's syndrome may be associated with small- or large-sensory nerve fibre damage. Small-fibre damage produces burning paraesthesias, whereas large-fibre damage produces ataxia or gait imbalance. Cranial neuropathies and autonomic neuropathy may also occur[35][36][37]
Sarcoidosis (neurosarcoidosis) can cause peripheral nerve damage, although facial palsy is the most common manifestation
Disorders of monoclonal protein production result in neuropathy due to protein deposition and inflammation in the peripheral nerves. Disorders include Waldenstrom's macroglobulinaemia, monoclonal gammopathy of uncertain significance, multiple myeloma, cryoglobulinaemia, and amyloidosis
Neuro-Behcet's disease can rarely present with spinal cord inflammatory lesions causing paraesthesias and weakness in the extremities[38]
Wartenberg’s migrant sensory neuritis is a limited, immune-mediated, mononeuritis affecting sensory nerves only. Presents with abrupt onset of painful paraesthesias in the distribution of one or multiple cutaneous or sensory nerves (most commonly peripheral limb nerves, but also the trigeminal nerve and truncal branches), either sequentially or simultaneously. Paraesthesias can be preceded by painful sensations (stabbing, burning, tingling) in the same area, and stretching of the affected nerve (e.g., by kneeling) may precipitate symptoms.[39][40]
Genetic disorders
Inherited causes for peripheral sensory neuropathy may include genetic mutations that affect the structure of the nerve fibre, leading to peripheral neuropathy or plexopathy. The most common causes are the following.
Charcot-Marie-Tooth disease (hereditary motor and sensory neuropathy): caused by mutations that affect either myelin (producing demyelination) or formation of the axon (producing axonal neuropathy). The inheritance may be autosomal dominant or recessive, depending on the form. The key symptom is motor weakness, but sensory symptoms including paraesthesias also occur.
Hereditary sensory and autonomic neuropathy: this is a group of genetic disorders that produce autonomic dysfunction and analgesia. The inheritance may be autosomal dominant or recessive, depending on the form. Patients may present with painless injuries to their extremities (due to lack of sensation) or with burning paraesthesias in the extremities.
Hereditary neuropathy with liability to pressure palsies: an autosomal dominant condition caused by a deletion of a region on chromosome 17 that includes the PMP-22 gene. Patients present with relapsing and remitting symptoms of nerve entrapment. The syndrome may involve isolated or multiple compressive neuropathies or a brachial plexopathy depending on the peripheral nerve involved.
Inborn errors of metabolism produce defects in downstream metabolism and a build-up of upstream metabolic intermediates in the cytoplasm, leading to cellular damage. A peripheral neuropathy results either from axonal damage or from demyelination. Demyelination is usually produced by damage to Schwann cells, but may also be caused by defective myelin synthesis.
Adult polyglucosan body disease is a glycogen-branching enzyme deficiency. The deficiency leads to the formation of polyglucosan bodies within nerve fibres. These bodies are toxic and lead to nerve damage. The condition presents in mid-to-late adulthood with paraesthesias or sensory loss in the lower extremities, progressive upper and lower motor neuron dysfunction, sphincter dysfunction (incontinence), and dementia.[41] It is caused by multiple mutations in the GBE1 gene.[41][42]
Tangier's disease is caused by a defect in high-density lipoprotein production, leading to deposition of cholesterol esters and cellular toxicity in various tissues including peripheral nerve Schwann cells. Patients develop paraesthesias and motor weakness due to a sensori-motor peripheral neuropathy. Orange-coloured tonsils are characteristic of the disease. Some patients present in childhood with symptoms affecting the lower extremities, whereas others present later in later with symptoms affecting the upper extremities.[43][44]
Refsum's disease is a peroxisomal disorder that produces accumulation of phytanic acid. It presents at a young age with retinitis pigmentosa, peripheral polyneuropathy, and cerebellar ataxia.
Fabry's disease, due to alpha-galactosidase deficiency, is an X-linked recessive disorder of glycolipid storage that affects male patients from an early age (usually <10 years old). The involved gene is located on the long arm of the X chromosome, between Xq21.33 and Xq22. Associated systemic conditions include chronic renal insufficiency, early cardiac or cerebrovascular disease, and corneal opacifications. Female carriers may have milder symptoms, with onset later in life. The peripheral neuropathy affects small unmyelinated nerve fibres, thus burning paraesthesias are prominent symptoms, located in the hands, feet, and distal lower extremities. Patients may also report reduced sweat output. Patients also have angiokeratomas and characteristic darkening of their skin in a 'bathing suit' distribution due to a macular rash.[45]
Krabbe's disease or globoid cell leukodystrophy is an autosomal recessive disorder produced by deficiency of galactocerebrosidase enzyme. It leads to decreased formation of myelin in the CNS and peripheral nerves. Infantile-, juvenile-, and adult-onset forms of the disease exist. Infantile onset is the most severe and fatal. Patients present with burning paraesthesias and muscle weakness due to sensori-motor neuropathy. Some patients also develop cognitive impairment or upper motor neuron signs due to demyelination in the CNS.[46][47]
Friedreich's ataxia, caused by an expanded trinucleotide repeat sequence in the frataxin gene, presents with progressive limb ataxia and axonal sensory neuropathy with pyramidal tract signs (weakness and upgoing toes to plantar stimulation) in the setting of absent deep tendon reflexes, and cardiomyopathy. Clinical symptoms develop in childhood or young adulthood.
Adrenomyeloneuropathy is an X-linked recessive disorder that causes the abnormal accumulation of very-long-chain fatty acids. It primarily affects young adult males, although female carriers may also have neurological involvement, and presents primarily with spastic paraplegia, adrenal insufficiency, and, occasionally, peripheral neuropathy and myelopathy.[48][49]
Spinocerebellar ataxia syndromes are a group of autosomal dominant inherited neuro-degenerative conditions. Some subtypes are associated with sensory neuropathy (types 1 to 4, 8, 18, 23, 24, 15, 27) in addition to ataxia and other features such as pyramidal and extra-pyramidal dysfunction.
Niemann-Pick disease, or acid sphingomyelinase deficiency, can produce peripheral neuropathy and retinal abnormalities.[50] However, this presentation is unusual as most patients have shortened life spans and do not live long enough to develop these symptoms.
Subacute necrotising encephalomyelopathy (Leigh's disease) is a severe neuro-degenerative disease of infancy that can include peripheral neuropathy in addition to psychomotor delay, seizures, ophthalmoplegia, ataxia, dystonia, seizures, and vomiting.[51][52] The condition is usually fatal in infancy or early childhood.
Abetalipoproteinaemia, or Bassen-Kornzweig syndrome, is an autosomal recessive disorder of defective lipoprotein metabolism and may present with sensory neuropathy in childhood in addition to other neurological features such as intellectual disability, retinitis pigmentosa, and ataxia.[53]
Other causes
Focal seizures (formerly known as partial seizures)
Focal seizures involving the somatosensory cortex may cause stereotyped hemifacial or hemibody sensory symptoms such as paraesthesias.
Paraneoplastic sensory neuropathy
A range of cancers can lead to a peripheral neuropathy. The cause is usually related to nerve entrapment by the tumour, side effects of treatment, nutritional deficiencies, or metabolic derangements. However, some patients develop a paraneoplastic peripheral neuropathy in the absence of these causes, which occurs in association with a variety of anti-neuronal antibodies including anti-Hu and anti-CRMP-5. The neuropathy may precede the diagnosis of cancer by many years and be the only clinical indication of an occult malignancy. The exact mechanism is not understood but is thought to be related to cross-reactivity of the anti-neuronal antibodies with tumour antigens.
Numb chin syndrome
Unilateral paraesthesias or anaesthesia of the chin may present as an initial manifestation of occult malignancy and should always be investigated thoroughly as to the underlying cause.[12][54] It may also be the initial manifestation of multiple sclerosis. It may also occur subsequent to dental or oral surgery.
Peripheral neuropathy after bariatric surgery
Sensory predominant, distal polyneuropathy has been found to occur more frequently in patients after bariatric surgery compared with other types of abdominal surgery.[55] Malnutrition related to the perioperative period seems to be the most significant risk factor for development of predominantly sensory, distal polyneuropathy.[55] Rapid loss of a large amount of body weight most likely results in several nutritional deficiencies, and subsequently the development of the polyneuropathy.
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