Paresthesia; Causes, Symptoms, Diagnosis, Treatment

Paresthesia is an abnormal sensation such as tingling, tickling, pricking, numbness or burning of a person’s skin with no apparent physical cause.  These sensations may be felt in the fingers, hands, toes, or feet. Depending on the cause, the sensation of paresthesia can be short-term and disappear quickly, such as when it occurs due to hyperventilation, an anxiety attack or from lying on the arm while asleep. Most people have experienced temporary paresthesia, a feeling of pins and needles, at some time in their lives when they have sat with legs crossed for too long, or fallen asleep with an arm crooked under their head. It happens when sustained pressure is placed on a nerve. The feeling quickly goes away once the pressure is relieved.

Paresthesia is an altered sensation of the skin, manifesting as numbness, partial loss of local sensitivity, burning, or tingling [rx]. Facial paresthesia has a known etiology in 83% of cases, and 48% of these have been attributed to a dental procedure [rx]. In paresthesia resulting from dental procedures, the inferior alveolar nerve (IAN) and lingual nerves are the most commonly implicated nerves [rx,rx].

Types of Paresthesia

The peripheral sensory nerves carry varied sensations from different regions of the body to the spinal cord. The signals are then directed from the spinal cord to the brain with the aid of the brain stem and trigeminal nerve. Any kind of problem or abnormality in this path can cause paresthesia.

Paresthesia may either occur spontaneously or due to a disease.

Transient(highly common)

• Common in the hands, arms, feet and legs
• Spontaneous and temporary
• Sustained pressure applied over a nerve, resulting to stimulated or inhibited function

Chronic or intermittent

• Due to poor circulation or ill-functioning neurons
• Often related to peripheral nervous system
• Paresthesia as a symptom of an underlying traumatic nerve damage or neurological disease
• Does not go away

Causes of Paresthesia

When a person experiences paresthesia, symptoms from a wide-range of possibilities may occur. There are a number of potential causes as well; multiple sclerosis for instance. The list below includes many of the potential causes of paresthesia.

Nerve demyelination and/or axonal degeneration

Multiple sclerosis

• A relapsing and remitting focal inflammatory disorder of the CNS clinically defined by two episodes of neurologic 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 paresthesias. Rarely, a patient may present with numb chin syndrome as an early manifestation of multiple sclerosis, where there are unilateral chin paresthesias.

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.

Guillain-Barre syndrome

• A demyelinating polyneuropathy characterized by an immune-mediated attack on the myelin sheath or Schwann cells of sensory and motor nerves. Several forms exist that are classified according to symptoms. 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 paresthesias in the feet and hands.

Chronic inflammatory demyelinating polyradiculoneuropathy

• An acquired, demyelinating, peripheral neuropathy of presumed autoimmune etiology. 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.

Diagnosis of Common Nerve Entrapment Syndromes
Syndrome	Nerve	Associated conditions	History	Physical examination
Carpal tunnel	Median nerve at wrist	Diabetes, pregnancy, rheumatoid arthritis, hypothyroidism, repetitive wrist movements, sustained hand positions, amyloidosis, acromegaly, multiple myeloma, chronic renal failure, tenosynovitis	Intermittent hand pain or paresthesias, especially at night; poor grip/dropping things; decreased fine motor skills	Decreased thumb adduction, thenar atrophy, decreased sensation of digits 1, 2 and 3, positive Phalen’s sign, positive Tinel’s sign
Cubital tunnel	Ulnar nerve at elbow	Leaning on elbow, shallow ulnar groove, increased forearm flexion/extension, elbow fracture, rheumatoid arthritis, immobilization	Elbow pain, hand weakness, numbness of ulnar side of hand	Decreased finger abduction, decreased thumb adduction, atrophy of intrinsic hand muscles (if severe), claw hand (if severe), decreased sensation of digits 4 (ulnar side) and 5, positive Tinel’s sign at elbow
Meralgia paresthetica	Lateral femoral cutaneous nerve	Obesity, pregnancy, diabets, increased walking/standing	Numbness/pain of lateral thigh	Usually no motor deficit, increased light touch and pinprick response over lateral thigh
Tarsal tunnel	Posterior tibial nerve	Phlebitis, rheumatoid arthritis, fracture	Burning/tingling of ankle and sole, increased with ambulation	Usually no motor deficit, decreased sensation on plantar foot, positive Tinel’s sign of nerve

Chronic inflammatory demyelinating sensory polyradiculopathy

• An acquired demyelinating condition that preferentially affects large myelinated fibers of the posterior roots. Presents with gait ataxia, large-fiber sensory loss, and paresthesias.
  

  Selected Causes of Paresthesias
  Central Ischemic Cerebrovascular accident Transient ischemic attack Structural Tumor Trauma Infectious Brain abscess Encephalitis	Inflammatory Systemic lupus erythematosus Nutritional Vitamin B12deficiency Miscellaneous Multiple sclerosis Peripheral Neuropathy

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 fibers exclusively, but more commonly involves both large and small sensory and motor nerve fibers. 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.

Endocrine or metabolic disease

Diabetes mellitus

• Hyperglycemia initiates a process of nerve damage affecting peripheral nerve fibers 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 ischemia of nerve trunks and ganglia. These changes impair mitochondrial function and neurotrophic support. Ongoing hyperglycemia produces progressive damage and loss of peripheral nerve fibers and impaired sensory function.

Uremia

• A clinical syndrome of metabolic abnormalities and fluid, electrolyte, and hormone imbalance that develops in the context of deteriorating renal function. Patients develop a generalized 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. Uremic encephalopathy may also occur.

Hypocalcemia

• Calcium plays a crucial role in neural function, and hypocalcemia produces a range of neurologic signs and symptoms including paresthesias affecting the fingertips, toes, and perioral region.

Hypothyroidism

• Produces a peripheral neuropathy with paresthesias, 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

• Vitamin B12 is critical in the production of S-adenosylmethionine, which is thought to be important in neural function. It is also an essential cofactor in hematopoiesis. Vitamin B12 deficiency usually manifests as a macrocytic anemia with or without paresthesias, but paresthesias 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

• Vitamin B6 is an important cofactor in amino acid and glycogen metabolism. Neurologic symptoms are wide ranging and include distal limb numbness, paresthesias, and weakness with impaired vibration and proprioception and sensory ataxia. Other signs include seborrheic dermatitis, atrophic glossitis with ulceration, and angular cheilosis.

Vitamin B1 deficiency

• Thiamine is an important cofactor 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

• 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

• Copper deficiency produces anemia 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 etiology 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.

Diagnosis of Common Nerve Root Lesions
Nerve root Disc level	C5 C4-C5	C6 C5-C6	C7 C6-C7	L4 L3-L4	L5 L4-L5	S1 L5-S1
Sensory	Lateral border of upper arm	Lateral forearm, including thumb, index finger and half of middle finger	Middle finger	Medial leg and medial foot	Dorsum of foot	Lateral foot
Reflex	Deltoid tendon	Biceps and brachioradialis tendon	Triceps tendon	Patellar tendon	None	Achilles tendon
Muscle	Deltoid, biceps	Wrist extensors, biceps	Triceps, wrist flexors, finger extensors	Inversion of foot	Dorsiflexion of toes and foot	Plantar flexion and eversion of foot

• Initially, patients develop numbness of the soles, followed by paresthesias of feet and legs, especially at night. Paresthesias slowly progress proximally, and become painful (described as burning or lancinating). Paresthesias 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). Paresthesia 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.

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. Mercury is used in some dental amalgams, and there is increasing concern about mercury exposure from contaminated fish.

Hexane

• Hexane, from glue-sniffing behavior 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 odorless 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 paresthesias, abdominal pain, nausea, vomiting, diarrhea, 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 paresthesias 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

• Postradiation-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.

Macrovascular disease

Stroke or TIA

• An ischemic or hemorrhagic stroke in the somatosensory cortex may cause paresthesias 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 paresthesias as the only manifestation.

Migraine

• Some migraine headaches are associated with an aura that includes focal or unilateral neurologic symptoms. These may include paresthesias 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).

Peripheral vascular disease

• Paresthesia is one of the classic signs of limb ischemia, along with pain, pallor, cold, absent pulses, and paralysis. The paresthesia is usually in a “glove and stocking” distribution.

Other cerebrovascular disease

• Unilateral paresthesias may rarely be associated with other vascular abnormalities in the brain and spinal cord, including cavernous malformations and intravascular lymphoma. Cavernous malformations most often occur in the brain but can also rarely affect extracranial areas such as the spinal cord, leading to paresthesias in the extremities.  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. Neurologic symptoms include sensory and motor neuropathies, paresthesia, muscle weakness, hemiparesis, meningoradiculitis, dysarthria, aphasia, seizures, transient visual loss, vertigo, and impaired cognitive function.
  

  Selected Causes of Peripheral Neuropathy
  Metabolic/nutritional disturbances Diabetes Hypothyroidism Vitamin B12 deficiency Alcoholism Uremia Amyloidosis Porphyria Entrapment syndromes Carpal tunnel syndrome Ulnar entrapment syndrome Thoracic outlet syndrome Lateral femoral cutaneous syndrome Peroneal palsy Tarsal tunnel syndrome Trauma Inflammation Acute idiopathic polyneuritis Chronic relapsing polyneuropathy	Connective tissue disorders Polyarteritis nodosa Autoimmune vasculitis Rheumatoid arthritis Systemic lupus erythematosus Systemic sclerosis Sjögren’s syndrome Toxins Chemotherapy Heavy metals Medications (didanosine [Videx], zalcitabine [Hivid], stavudine [Zerit]) Industrial exposures Chronic overdosage of pyridoxine Hereditary conditions Charcot-Marie-Tooth disease Denny-Brown’s syndrome Familial amyloiditic polyneuropathy	Malignancy Tumor compression Paraneoplastic syndromes Lymphomas Cancer of the lung, stomach, breast or ovary Plasma cell dyscrasias Multiple myeloma Osteoclastic myeloma Monoclonal gammopathy Waldenstrom’s macroglobulinema Miscellaneous Sarcoidosis Malnutrition Infections Lyme disease HIV infection Leprosy

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. CMV can produce a polyradiculopathy in immunosuppressed patients, especially those with AIDS.

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 paresthesia. These are shortly followed by a characteristic rash in the affected dermatome.

Herpes simplex infection

• Causes oral, genital, and ocular ulcers. Patients report a localized paresthesia that forms part of the prodrome prior to the onset of the ulcers. The paresthesia may be the only symptom in some patients.

Neurosyphilis

• An STD caused by Treponema pallidum. Associated with primary (local), secondary (disseminated), and tertiary (end-organ complications including neurosyphilis) disease. 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 paresthesias that are associated with anxiety or panic symptoms and hyperventilation. An extremely common cause of paresthesias.

Conversion and somatization disorders

• Caused by an underlying psychiatric condition. The distribution of the paresthesias may be focal or hemifacial or hemibody, but does not correlate with a pathologic 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.  Peripheral sensory neuropathy may also occur due to direct immune-mediated nerve inflammation caused by autoantibodies or a reaction to monoclonal protein deposition. In some cases, a combination of these etiologies is present. Causes include:

• Vasculitis associated with connective-tissue diseases such as SLE and rheumatoid arthritis. SLE is associated with a distal symmetric sensory neuropathy with progressive distal lower extremity paresthesias, which may progress to involve motor nerve fibers
• 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 ischemia, and renal failure.
• Churg-Strauss syndrome, a vasculitic condition that affects small- and medium-sized blood vessels. Associated abnormalities include asthma, eosinophilia, and abnormal infiltrates on CXR.
• Granulomatosis with polyangiitis (Wegener), a vasculitis affecting small- and medium-sized blood vessels with lesions of the nasal passages, lungs, and kidney.
• 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 syndrome may be associated with small- or large-sensory nerve fiber damage. Small-fiber damage produces burning paresthesias, whereas large-fiber damage produces ataxia or gait imbalance. Cranial neuropathies and autonomic neuropathy may also occur.
• 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 macroglobulinemia, monoclonal gammopathy of uncertain significance, multiple myeloma, cryoglobulinemia, and amyloidosis.
• Neuro-Behcet disease can rarely present with spinal cord inflammatory lesions causing paresthesias and weakness in the extremities.
• Wartenberg migrant sensory neuritis is a limited, but immune-mediated, mononeuritis affecting sensory nerves only. Presents with abrupt onset of painful paresthesias 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. Paresthesias 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.

Genetic disorders

Inherited causes for peripheral sensory neuropathy may include genetic mutations that affect the structure of the nerve fiber leading to peripheral neuropathy or plexopathy. The most common causes are:

• 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 paresthesias 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 paresthesias 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 buildup of upstream metabolic intermediates in the cytoplasm. Either effect can lead 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 fibers. These bodies are toxic and lead to nerve damage. The condition presents in mid-to-late adulthood with paresthesias or sensory loss in the lower extremities, progressive upper and lower motor neuron dysfunction, sphincter dysfunction (incontinence), and dementia.It is caused by multiple mutations in the GBE1 gene.
• Tangier disease is caused by a defect in HDL production, leading to deposition of cholesterol esters and cellular toxicity in various tissues including peripheral nerve Schwann cells. Patients develop paresthesias and motor weakness due to a sensorimotor peripheral neuropathy. Orange-colored tonsils are characteristic of the disease. Some patients present in childhood with symptoms affecting the lower extremities, whereas others present in later life with symptoms affecting the upper extremities.
• Refsum 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 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 fibers, thus burning paresthesias 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.
• Krabbe 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 paresthesias and muscle weakness due to a sensorimotor neuropathy. Some patients also develop cognitive impairment or upper motor neuron signs due to demyelination in the CNS.
• Friedreich 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 neurologic involvement, and presents primarily with spastic paraplegia, adrenal insufficiency, and, occasionally, peripheral neuropathy and myelopathy.
• Spinocerebellar ataxia syndromes are a group of autosomal dominant inherited neurodegenerative conditions. Some subtypes are associated with sensory neuropathy  in addition to ataxia and other features such as pyramidal and extrapyramidal dysfunction.
• Niemann-Pick disease, or acid sphingomyelinase deficiency, can produce peripheral neuropathy and retinal abnormalities.However, this presentation is unusual as most patients have shortened life spans and do not live long enough to develop these symptoms.
• Leigh subacute necrotizing encephalomyelopathy is a severe neurodegenerative disease of infancy that can include peripheral neuropathy in addition to psychomotor delay, seizures, ophthalmoplegia, ataxia, dystonia, seizures, and vomiting.  The condition is usually fatal in infancy or early childhood.
• Abetalipoproteinemia, 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 neurologic features such as mental retardation, retinitis pigmentosa, and ataxia.
• Some associate
• Condition that causes  paresthesia
• Entrapment of nerve
• Traumatic nerve damage
• Compression of nerve
• Peripheral neuropathy

Other causes may include

• Lidocaine poisoning
• Anticonvulsant drugs
• Lupus erythematosus
• Neurological disorders
• Motor neuron diseases
• Lyme disease infection
• Beta-alanine ingestion
• Autoimmune disorders
• Heavy metal poisoning
• Guillain-Barre Syndrome
• Encephalitis
• Arteriovenous malformation – pressing against CNS and brain
• Diabetic neuropathy
• Diabetes
• Vitamin B12 deficiencies
• Hypothyroidism
• Alcoholism
• Heavy metal poisoning
• Arsenic poisoning
• Lead poisoning
• Carpal tunnel syndrome
• Nerve entrapment syndromes
• Rheumatoid arthritis
• Systemic lupus eruthematosus

Chronic paresthesia causes

It can be caused due to deadly underlying conditions. Untreated cases can lead to development of life-threatening complications. Some of the known causes of chronic paresthesia are listed

• Different kinds of thyroid disorders as well as presence of hormonal conditions such as menopause
• Some of the main causes of chronic paresthesia include autoimmune disorders such as rheumatoid arthritis, pernicious anemia, diabetes, and lupus or systemic lupus erythematosus.
• Abnormalities associated with circulatory diseases such as Raynaud’s disease, acute arterial occlusion, and atherosclerosis have been found to cause chronic paresthesia in many people. It is also one of the main causes of facial paresthesia.
• Tingling, numbness, and burning sensations in feet can also arise due to deficiencies in different vitamins like B1, B5, and B12.
• Other probable causes include disorders of the spinal cord and/or brain, brain tumors, etc.
• Certain kinds of treatment like radiation therapy or chemotherapy
• Perioral paresthesia has been found to have links with hypocalcaemia.
• Different kinds of infections, including herpes zoster virus, HIV/AIDS, Lyme disease, and herpes simplex virus, etc.
• Chronic paresthesia may also be caused by varied anomalies like blood diseases, a weakened immune system, skin conditions, and joint and bone disorders, etc.
• Consumption of certain medicines such as mefloquine, dimercaprol, riluzole, lomotil, and anticonvulsant drugs, etc. can also trigger an episode of chronic paresthesia.
• Poisoning by toxic chemicals or heavy metals, or exposure to radiation
• Presence of inherited disorders such as Fabry disease, Refsum syndrome, and Charcot-Marie-Tooth disease can also increase the vulnerability to developing chronic paresthesia.
• Intake of illegal drugs, excessive alcohol, and smoking are other causes
• Chronic paresthesia can also occur due to continuous or lasting damage to the nerves caused by different conditions like meralgia paresthetica, carpal tunnel syndrome, a pinched nerve in the spine, a transient ischemic attack or stroke, transverse myelitis, and multiple sclerosis.

Drugs Causing Neuropathies

Axonal

Vincristine

Paclitaxel

Nitrous oxide

Colchicine

Isoniazid

Hydralazine

Metronidazole

Pyridoxine

Didanosine

Lithium

Alfa interferon

Dapsone

Phenytoin

Cimetidine

Disulfiram

Chloroquine

Ethambutol

Amitriptyline

Demyelinating

Amiodarone

Chloroquine

Suramin

Gold

Neuronopathy

Thalidomide

Cisplatin

Pyridoxine

Symptoms of Paresthesia

Interestingly, paresthesia itself is something that can be considered a symptom of certain conditions.  In addition, the paresthesia a person experiences may be either chronic or transient. When paresthesia is caused by a particular condition, additional symptoms might become a part of the person’s experience, related to underlying causes. The symptoms of paresthesia may include:

• Itching
• Tingling
• Footdrop
• Dysarthria
• Numbness
• Muscular atrophy
• Ocular Dysmetria
• Restless leg syndrome
• Crawling sensation on the skin
• “Falling asleep” of limbs such as a hand, foot, arm, leg, etc.

Diagnostic Tests

Hyperthyroidism	EMG and nerve conduction studies: distal sensorimotor peripheral neuropathy, mixed axonal and demyelinating; may have focal superimposed mononeuropathies such as median neuropathy at the wrist thyroid function tests: increased TSH and low free T4 in primary hypothyroidism; low or normal TSH and low free T4 in secondary hypothyroidism
Vitamin B1 deficiency	therapeutic trial of thiamine supplementation: symptoms resolve in vitamin B1 deficiency 24-hour urine thiamine excretion: reduced in vitamin B1 deficiency serum thiamine level: reduced in vitamin B1 deficiency serum pyruvate: increased in vitamin B1 deficiency	EMG and nerve conduction studies: sensorimotor peripheral neuropathy transketolase activity in whole blood or RBC: enzyme activity increases after addition of thiamine in vitamin B1 deficiency
Vitamin B6 deficiency or excess	serum vitamin B6 level: reduced in vitamin B6 deficiency; elevated with excess	EMG and nerve conduction studies: may demonstrate a sensory greater than motor peripheral neuropathy
Vitamin B12 deficiency	serum vitamin B12 level: <300 picogram/mL serum methylmalonic acid: elevated serum homocysteine level: elevated	EMG and nerve conduction studies: sensorimotor peripheral neuropathy MRI of spinal cord: may show increased signal on T2-weighted images in the dorsal and lateral columns of the spinal cord in cases with subacute combined degeneration
Vitamin E deficiency	serum vitamin E: <0.5 mg/dL	EMG and nerve conduction studies: may show sensory neuropathy, worse in the lower extremities somatosensory-evoked potentials: may show slowing of conduction of evoked potentials at the spinal cord level
Drug toxicity	trial of discontinuation of causative medication: symptoms resolve
Alcoholic neuropathy	EMG and nerve conduction studies: axonal sensorimotor peripheral neuropathy	LFTs: normal or elevated gamma-GT, AST, and ALT (with AST>ALT)
Stroke/transient ischemic attack	CT scan of head: may appear normal initially or show acute intraparenchymal ischemic infarct (hypodensity) or hemorrhagic infarct (hyperdensity) MRI of brain: acute infarction (hemorrhagic or ischemic) in 1 or more cerebrovascular territories	MR angiogram of Circle of Willis and neck: focal stenosis of medium- to large-diameter intracranial and extracranial blood vessels; acute dissection of arterial walls (internal carotid, vertebral) in head and neck can produce thrombi that may block blood flow and cause an acute ischemic intraparenchymal infarct or transient cerebral ischemia; acute dissection may occur spontaneously or following minor head/neck trauma or repositioning, and neck/head pain may or may not be present; [64] proceed with 4-vessel cerebral arteriography (or CT angiogram) if there is high suspicion for a vascular etiology for a cerebral infarct or transient cerebral ischemia, and initial imaging is negative; fibromuscular dysplasia of the carotid or vertebral arteries may also cause ischemic stroke in young adults, and may be diagnosed using one of these techniques CT angiogram of head and neck: to detect arterial dissection when cerebral arteriography is not available emergently, or there are contraindications to cerebral angiogram (contrast dye allergy, renal insufficiency)
Migraine with aura	clinical diagnosis	MRI brain: may be normal or demonstrate mild subcortical white matter changes (chronic), if history of prior migraine headache
Peripheral vascular disease	ankle brachial index: ≤0.90	segmental pressure examination: gradient of >20 mmHg between adjacent segments duplex ultrasound: peak systolic velocity ratio >2.0 angiography: artery stenosis
Panic attack with hyperventilation	clinical diagnosis	trial of hyperventilation for 1 to 2 minutes: reproduces symptoms EMG and nerve conduction studies: normal
Charcot-Marie-Tooth disease	EMG and nerve conduction studies: varies depending on type; type 1: severe demyelinating neuropathy with conduction velocities in the 10 to 20 m/second range (cut-off 38 m/second); type 2: relatively preserved conduction velocities (cut-off 38 m/second) but low sensory and motor nerve amplitudes genetic testing: identification of causative mutations; type 1: duplication of PMP 22 gene on chromosome 17p11.2, MPZ, connexin32 or mutations P0; type 2: mitofusin2, RAB7 mutations	sural nerve biopsy: type 1: onion bulb formation and demyelination; type 2: chronic axonal degeneration
Hereditary sensory and autonomic neuropathy (HSAN)	EMG with nerve conduction studies: sensorimotor peripheral neuropathy with predominant sensory component	autonomic function testing: generalized autonomic failure including sudomotor, cardiovagal, and adrenergic dysfunction genetic testing: identified mutation in HSAN type 1 (most common) in serine palmitoyltransferase (SPTLC1) at chromosome 9q221-q22.3
Hereditary neuropathy with liability to pressure palsy (HNPP)	EMG and nerve conduction studies: generalized, mild, demyelinating sensorimotor peripheral neuropathy with superimposed focal mononeuropathies at common sites of compression genetic testing: deletion of chromosome 17p11.2	sural nerve biopsy: tomacula or reduplication of myelin around axons and demyelination

Uncommon

Differential	1st Tests	Other Tests
Brachial plexopathy	EMG and nerve conduction studies: asymmetric abnormalities in sensory and motor nerve conduction studies in the affected limb; no involvement of corresponding paraspinal muscles MRI of the brachial plexus or lumbosacral plexus (pelvis and hip): increased signal and abnormal enhancement in a patchy pattern; possible mass lesion (tumor or retroperitoneal hematoma) impinging on plexus	CXR: elevated hemidiaphragm on side of affected limb more peripheral nerve biopsy: perivascular inflammation; may also show perineurioma or lymphomatous or carcinomatous infiltration
Lumbosacral plexopathy	EMG and nerve conduction studies: asymmetric abnormalities in sensory and motor nerve conduction studies in the affected limb; no involvement of corresponding paraspinal muscles MRI of the brachial plexus or lumbosacral plexus (pelvis and hip): increased signal and abnormal enhancement in a patchy pattern; possible mass lesion (tumor or retroperitoneal hematoma) impinging on plexus	peripheral nerve biopsy: perivascular inflammation; may also show perineurioma or lymphomatous or carcinomatous infiltration
Tibial neuropathy	EMG and nerve conduction studies: asymmetry between the affected and unaffected leg with tibial motor nerve conduction studies with recording from the abductor hallucis and the abductor digiti quinti minimi muscles; prolonged distal latencies and/or reduced or absent medial and lateral plantar sensory potentials on the affected foot	MRI of ankle joint: often normal; may show enlargement of tibial nerve in the tarsal tunnel or increased signal in adjacent connective tissue suggestive of localized inflammation
Trigeminal Neuropathy	MRI brain with and without contrast: abnormal signal or contrast enhancement of ipsilateral trigeminal nerve or its ganglia	EMG and nerve conduction studies: decreased trigeminal nerve function detected by blink reflex testing on affected and unaffected sides
Acute Demyelinating Encephalomyelitis	MRI brain and spinal cord, with and without contrast: multifocal deep subcortical white matter lesions with increased signal intensity on T2-weighted and fluid-attenuated inversion recovery sequences; may enhance with contrast administration or contain hemorrhage in acute setting LP with CSF exam: pleocytosis, increased protein level, abnormal immunoglobulin production (IgG index), and presence of oligoclonal bands
Guillian-Barre Syndrom	LP with CSF exam: albuminocytologic dissociation (elevated CSF protein with normal WBC and RBC counts) EMG and nerve conduction studies: demyelinating sensorimotor peripheral neuropathy with prolonged F-wave and distal sensory and motor latencies; relative preservation of sensory and motor nerve amplitudes	anti-GQ1b antibody: may be elevated in patients with extraocular muscle weakness (Miller-Fisher variant)
Chronic Inflammatory Demyelinating Polyneuropathy (CIDP)	EMG and nerve conduction studies: demyelinating sensorimotor peripheral neuropathy with prolonged distal latencies and slowed conduction velocities; relative preservation of amplitudes LP with CSF exam: albuminocytologic dissociation (elevated CSF protein with normal WBC and RBC counts)	anti-myelin-associated protein antibody: may have positive or elevated titers in serum with certain subtypes of CIDP anti-GMI antibody: may have positive or elevated titers in serum with certain subtypes of CIDP serum protein electrophoresis with immunofixation: monoclonal protein spike with certain subtypes of CIDP
Chronic inflammatory demyelinating sensory polyradiculopathy (CISP)	MRI of spine, with and without contrast: diffuse enlargement and abnormally increased signal and contrast enhancement of multiple dorsal nerve roots EMG and nerve conduction studies: usually normal somatosensory-evoked potentials from the upper and lower extremities: delayed conduction of potentials through the spinal cord; demonstrates the site of the pathology, which is the dorsal sensory root	LP with CSF exam: albuminocytologic dissociation (elevated CSF protein with normal WBC and RBC counts)
Uremia	serum creatinine: elevated creatinine clearance: <10 mL/min	EMG and nerve conduction studies: axonal sensorimotor polyneuropathy
Hypocalcemia	serum calcium: reduced serum vitamin D: reduced in vitamin D deficiency serum parathyroid hormone: reduced in hypoparathyroidism; elevated in pseudohypoparathyroidism serum magnesium: may be reduced
Copper deficiency	serum copper: decreased serum zinc: increased in zinc toxicity EMG and nerve conduction studies: may show sensory neuropathy	somatosensory-evoked potentials: delay of conduction of nerve potentials at the level of the spinal cord
Heavy metal poisoning	EMG and nerve conduction studies: axonal sensorimotor polyneuropathy whole blood lead level: elevated in lead exposure 24-hour urine test for arsenic, mercury, thallium: elevation of relevant heavy metal	hair and fingernail arsenic level: positive in arsenic exposure
Radiation	EMG and nerve conduction studies: asymmetric abnormalities in sensory and motor nerve conduction studies in the affected limb; no involvement of corresponding paraspinal muscles; myokymia (localized muscle quivering) on needle EMG exam of muscles in affected extremity MRI of the brachial plexus or lumbosacral plexus (pelvis and hip): increased signal and abnormal enhancement in a patchy pattern	CXR: elevated hemidiaphragm on side of affected limb in brachial plexopathy more peripheral nerve biopsy: perivascular inflammation
Hexane	EMG and nerve conduction studies: axonal sensorimotor peripheral neuropathy urine hexanediol and hexenol level: elevated
Ciguatera or saxitoxin poisoning	EMG and nerve conduction studies: axonal sensorimotor peripheral neuropathy testing for serum ciguatera toxin or saxitoxin: positive if ingested
HIV neuropathy	HIV antibody: positive EMG and nerve conduction studies: distal axonal sensorimotor peripheral neuropathy
Leprosy	skin smear: isolation of Mycobacterium leprae	sural cutaneous nerve biopsy: may show mixture of axonal and demyelinating abnormalities; infectious organism may be found within Schwann cells EMG and nerve conduction studies: may show distal sensorimotor peripheral neuropathy with superimposed mononeuropathies (ulnar, median, fibular [peroneal], tibial)
Herpes simplex infection	viral culture: virus detected HSV PCR: positive serum anti HSV-1 and HSV-2 antibodies: positive for causative virus
Neurosyphilis	EMG and nerve conduction studies: sensory greater than motor peripheral neuropathy serum RPR test: positive serum VDRL test: positive	LP with CSF exam: normal or may show mildly elevated protein and mild pleocytosis CSF VDRL: positive more
Herpes zoster infection (shingles)	clinical diagnosis	PCR of lesions: positive for varicella zoster virus
Lyme disease	serum ELISA: positive more	EMG and nerve conduction studies: may show distal sensorimotor peripheral neuropathy, multiple mononeuropathies, or radiculoneuropathy LP with CSF exam: may show elevated protein or mild lymphocytosis; positive Lyme antibody titers
Conversion and somatization disorders	EMG and nerve conduction studies: normal
Inborn errors of metabolism	clinical picture screen for appropriate inborn error of metabolism: identification of underlying condition EMG and nerve conduction studies: sensory neuropathy; pattern depends on underlying cause	MRI brain: hyperintense confluent white matter lesions in both hemispheres in adult polyglucosan body disease genetic testing: identification of causative mutations
Rheumatoid arthritis	EMG and nerve conduction studies: multiple mononeuropathies with axonal features or axonal sensorimotor polyneuropathy serum rheumatoid factor: positive	cervical spine x-ray: may show atlantoaxial subluxation causing cervical spinal cord compression sural nerve biopsy: vasculitis
SLE	EMG and nerve conduction studies: distal sensorimotor peripheral neuropathy ANA: elevated titers, >1:80	anti-double-stranded DNA: elevated titers
Churg-Strauss syndrome	EMG and nerve conduction studies: axonal polyneuropathy or multiple mononeuropathies CBC with differential: eosinophilia, more than 10%	biopsy of skin lesions: inflammation with increased eosinophils sural nerve biopsy: epineurial vasculitis in nerve with increased eosinophils and CD8 and CD4 lymphocytes
Granulomatosis with polyangiitis (Wegener)	EMG and nerve conduction studies: multiple mononeuropathies with axonal loss antineutrophil cytoplasmic antibody antibodies: positive; subcomponents PR3 or MP0 also positive	CBC with differential: normocytic anemia; may have leukocytosis and thrombocytosis ESR: highly elevated CRP: highly elevated biopsy of affected tissue: vasculitis of medium and large vessels
Polyarteritis nodosa	EMG and nerve conduction studies: multiple mononeuropathies with axonal features peripheral nerve biopsy: vasculitis involving large-sized more than medium-sized blood vessels
Microscopic polyangiitis	EMG and nerve conduction studies: multiple mononeuropathies in the extremities with axonal features peripheral nerve biopsy: perivascular inflammation in the epineurium or endoneurium	ESR: normal or elevated CRP: normal or elevated
Sjogren syndrome	EMG and nerve conduction studies: patchy sensory greater than motor peripheral neuropathy is the most common pattern; may also have ganglionopathy or sensory neuronopathy with absence of sensory nerve responses and normal motor nerve conduction studies Schirmer test: severe dry eye serum anti-SSA and SSB antibodies: positive	quantitative sweat testing: patchy or length-dependent postganglionic sympathetic sudomotor nerve fiber dysfunction quantitative sensory testing: elevated vibratory and cooling detection thresholds; may have lowered heat-pain detection threshold and/or hypersensitivity to heat-pain testing if primarily small-fiber sensory neuropathy Rose-Bengal staining of eye: severe dry eye and reduced tear formation minor salivary gland lip biopsy: perivascular or periductal mononuclear cell infiltrates
Sarcoidosis	EMG and nerve conduction studies: axonal sensorimotor peripheral neuropathy; pattern may be multiple mononeuropathies, polyneuropathy, radiculopathy, or cranial neuropathy	sural nerve biopsy: multinucleated giant cells; granuloma with inflammatory perivascular infiltrates and axonal loss; negative for tuberculosis tissue biopsy: granuloma MRI of total spine: may show enlargement and abnormal enhancement of spinal nerve roots if radiculopathy is present CXR: hilar adenopathy or widening of the mediastinum tuberculin skin test with cutaneous anergy panel: negative
Monoclonal protein production	EMG and nerve conduction studies: demyelinating sensorimotor peripheral neuropathy or multiple mononeuropathies serum protein electrophoresis with immunofixation: monoclonal or biclonal IgM protein spike urine protein electrophoresis with immunofixation: free light chain (Bence-Jones) proteins or monoclonal proteins	serum amyloid free light chains: increase in free light chain (kappa and lambda) ratios in amyloidosis serum cryoglobulins: positive in cryoglobulinemia; pattern of monoclonal protein determines type hepatitis C antibodies: IgG or IgM titers may be positive in cryoglobulinemia beta-2-microglobulin: increased in Waldenstrom macroglobulinemia sural nerve biopsy: demyelination with IgM deposits and myelin lamellae in Waldenstrom macroglobulinemia; amyloid deposits surrounding endoneurial blood vessels in patients with amyloidosis; cryoglobulinemia may produce vasculitis affecting small-caliber blood vessels in epineurium or endoneurium
Partial epilepsy	EEG: interictal epileptiform discharges over the contralateral parietal lobe	MRI brain, with and without contrast administration: may show evidence of cortical-based lesion or scar, such as tumor or stroke
Paraneoplastic sensory neuropathy or ganglionopathy	serum anti-Hu and anti CV-2 antibodies: negative or positive EMG and nerve conduction studies: ganglionopathy produces absence of sensory nerve action potential responses diffusely; sensory neuropathy produces reduced sensory nerve amplitudes	mammogram: identification of breast cancer lesion CT scan of chest/abdomen/pelvis: identification of underlying malignancy whole-body PET scan: identification of underlying malignancy
Intravascular lymphoma	MRI brain: ischemic	brain biopsy: histopathologic evidence of lymphoma
Neuro-Behcet disease	MRI spinal cord: inflammatory lesions MRI brain with magnetic resonance angiography: findings can be similar to those in multiple sclerosis, or distinct white matter changes commonly involving midbrain
Wartenberg migrant sensory neuritis	clinical diagnosis	nerve conduction studies: sensory nerve action potential (SNAP) amplitude low in affected nerve or <50% of that on unaffected side; motor nerve conduction studies normal nerve biopsy: variable and nonspecific changes ranging from perineural inflammatory changes, changes more suggestive of non-systemic vasculitic neuropathy, to axonal degeneration as seen in ischemic neuronal lesions
Numb chin syndrome	MRI of brain and total spine: multiple sclerosis shows hyperintensities in the periventricular white matter, most sensitive images are sagittal fluid-attenuated inversion recovery, and demyelinating lesions in the spinal cord, particularly the cervical spinal cord mammogram: identification of breast cancer lesion CT scan of chest/abdomen/pelvis: identification of underlying malignancy	LP with CSF exam and culture: multiple sclerosis shows unique oligoclonal bands; increased IgG index; increased myelin basic protein; mild lymphocytic pleocytosis; testing for infectious agents is negative whole-body PET scan: identification of underlying malignancy
Peripheral neuropathy after bariatric surgery	EMG and nerve conduction studies: reduced or absent sensory nerve action potential and compound muscle action potential amplitudes in the lower extremities, with upper extremity nerves affected as polyneuropathy progresses proximally in the limbs; findings are symmetric in distribution; less likely prolongation of distal latencies or slowing of conduction velocities, but if present, also in a distal pattern; may be normal if only small diameter sensory nerve fibers involved clinically	serum vitamin B12: may show B12 deficiency serum folate: may show folate deficiency serum thiamine: may show thiamine deficiency serum vitamin B6: may show B6 deficiency CSF examination: with increased protein but normal WBC counts ESR: may be elevated quantitative sensory testing: may show elevated vibratory, cooling, and heat detection thresholds; heat detection threshold may be reduced in patients with small fiber sensory neuropathy who have allodynia autonomic reflex function testing (especially quantitative sweat testing): may show distal loss or reduction of sweat output, if small diameter, unmyelinated nerve fibers are affected thermoregulatory sweat testing: may be abnormal in the distal extremities, showing reduced sweating peripheral cutaneous nerve biopsy: may show active or chronic axonal degeneration; pathological evidence of an immune process with perivascular inflammatory mononuclear cell deposits
Notalgia paresthetica	clinical diagnosis	spinal MRI: consider if additional neurologic symptoms are present or current symptoms are progressive skin biopsy: may show focal inflammatory changes in affected skin

In further investigation are following

 Labs: Initial Evaluation

• Complete Blood Count
• Chemistry panel or metabolic panel
• Urinalysis
• Thyroid Stimulating Hormone (TSH)
• Erythrocyte Sedimentation Rate (ESR)

 Labs: Other Studies when indicated

• Dehydration
• Serum Folate
• Vitamin B12
• Syphilis Serology (VDRL or RPR)
• Antinuclear Antibody (ANA)
• Nerve conduction velocities
• Electromyogram (EMG)
• XRay of affected extremity
• Magnetic resonance imaging(MRI)
• Myelography
• Nerve biopsy
• Muscle biopsy
• Serum immunoelectrophoresis
• Purified Protein Derivative (PPD)
• VDRL
• Antinuclear antibodies
• Roentgenograms
• Computed tomographic scan
• Lumbar puncture
• Purified protein derivative (PPD)
• Heavy metal analysis

Treatment of Paresthesia

• Anti-inflammatory medication, such as NSAIDs  can help with the associated symptoms (pain relief, reduction of inflammation

• Antidepressant drugs  – recommended in low doses, so as to help modify the way the body perceives the pain (makes chronic conditions more bearable)

• Opiate medication  – recommended as a symptomatic treatment for the cases that are more severe (risk of addiction)

• Nutritional deficiencies can be corrected with vitamin supplements

• Immunosuppressants
• Gamma globulin – intravenous administration
• Anticonvulsants (gabapentin, gabitril, pregabalin)
• Antiviral medication – recommended in patients who suffer from paresthesia caused by shingles
• Topical numbing creams   – lidocaine or prilocaine creams (only the recommended amount should be applied, otherwise the excess of cream can actually cause paresthesia)
• Baclofen (high dosage) – recommended in patients who suffer from paresthesia caused by stroke; high doses of Baclofen are required to be administered several times per day (temporary relief)
• Cannabis – this is not an approved treatment but it is often used by those who suffer from HIV/AIDS (temporary relief from the experienced symptoms)

Acute Paresthesia Treatment

1. Caused by pressure to the nerve

• Massaging, exercising or stretching the limbs affected

Stretching and exercising as relief for paresthesia

• Refrain from crossing legs

2. Anxiety/Panic attack

• If paresthesia is caused by anxiety attack, it will be gone when the episode ends.

Chronic Paresthesia Treatment

1. Tight Cast

• Cutting and opening of the cast to relieve pressure put on the nerves.

2. Cardiovascular Causes

• The focus of treatment in paresthesia caused by cardiovascular diseases would be controlling two factors. These are cholesterol levels and blood pressure.

3. Diabetic neuropathy

• Regular monitoring which involves controlling of the blood sugar levels
• Medications
• Diet appropriate for people with diabetes

4. Vitamin B12 deficiency

• Nutritional therapy (B complex supplements)

5. Medications for specific conditions

• Immunosuppressants such as prednisone
• Anticonvulsants like Gabapentin
• Antiviral medications for paresthesia caused by shingles
• Intravenous gamma globulin (IVIG)

6. Topical creams

These are given as a palliative treatment. Usually, these topical creams can cause numbing to relieve the sensation of paresthesia. These include:

• Lidocaine creams
• Prilocaine creams

7. Other forms of treatment for chronic causes of paresthesia are

• Surgical interventions
• Physical and occupational therapy: Involves helping the patient perform activities of daily living (ADLs), use of assistive/orthopedic devices.
• Changes in lifestyle and diet: includes refraining from alcohol consumption and intake of vitamin supplement

Alternative treatment

• Acupuncture: Believed to relieve paresthesia
• Self-massage: Ideally done with aromatic oils.
• Application of capsaicin-containing ointments also helps in resolving paresthesia.
• Stress management and adequate hours of sleep
• Exercise regimen
• Wearing appropriate and loose-fitting shoes and clothes.

As it was mentioned, paresthesia is a symptom and not a condition on its own. This is the reason why the treatment mainly addresses the underlying condition. Once the condition behind the paresthesia has been successfully treated, the tingling or numbness sensation is going to disappear on its own.

These are the general measures that can be taken in order to improve the paresthesia:

• Avoid periods of prolonged sitting (especially with the legs crossed)
• If you do have to sit for prolonged periods of time, make sure that you stretch or massage the legs
• The tingling or numbness sensation can be improved through self-massage – it is recommended that the message is either performed with aromatic oils or by using specialized ointments (such as capsaicin); this message can provide temporary relief from the paresthesia sensation

Natural Remedies For Tinglings In Hands And Feet

Now that we know about the causes, let’s look at some home remedies for tingling and numbness! Next time you get that ‘pins and needles’ sensation, you can try one of these simple tips!

Move Around

• Usually, tingling sensation and numbness are caused by sitting in the same position for long stretches of time. The best treatment for this is trying some basic stretches or exercising a little to improve blood circulation.

Correct Posture

• Often our incorrect posture or lack of movement can trigger numbness and tingling. Awkward posture can restrict blood circulation, which leads to numbness. Incorrect posture can also lead to back pain and tingling sensations in the bladder or abdomen. So the next time you are on the computer or are watching television, be sure to maintain the right posture.

Rest

• Continuous activity can also trigger tingling in the feet and arms. So, the best way to treat such cases is to lie down and take a nice rest.

Yoga/Physiotherapy

• One of the best ways to ease tingling sensation and numbness is regularly practicing yoga. Yoga helps calm the body and mind, and at the same time also helps enhance and stimulate healthy blood circulation. Thus, it can significantly help reduce tingling and numbness.

Vitamin B- Complex

• This is one of the best home remedies for episodic or chronic tingling or numbness. A lack of vitamin B12 is one of the most common reasons for chronic tingling and numbness

Avoid Caffeine

• Another remedial action you can take is avoiding excessive coffee consumption. Caffeine dehydrates the body and impedes blood circulation, thereby leading to numbness and tingling. Thus, avoid caffeine and avoid tingling.

Include Magnesium In Diet

• Magnesium is an essential mineral that not only solves problems like insomnia but also helps the nervous and cardiovascular system function optimally. You can consider supplementing your diet with magnesium, as it helps enhance blood circulation, which in turn lessens tingling and numbness.

Lower Blood Sugar

• Another cause for tingling and numbness is diabetes. A common condition associated with diabetes, called diabetic neuropathy, can lead to pain, tingling, and numbness in the fingers and toes. So, try and eat foods that help you lower blood sugar.

Limit Alcohol

• Although you might be quite fond of your weekly glass of wine, you might want to consider giving it up. Studies prove that tingling and numbness can also be caused by alcoholism. Thus, one of the best ways to reduce the feeling is to limit the amount of alcohol you put into the system.

We hope that these remedies will help you get rid of that irritating tingling sensation! To tell us about any other activities that you use to get rid of this condition, share your experiences here. Leave a comment below!

References

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