Parasthesia
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Paresthesia
Definition
Paresthesia is an abnormal, spontaneous sensation arising without an external stimulus. It includes tingling, "pins and needles," prickling, burning, or crawling sensations. It is a positive sensory symptom - in contrast to numbness (loss of sensation), which is a negative symptom.
- Dysesthesia - an abnormal perception evoked by a stimulus (e.g., pressure producing tingling or pain). If large-diameter axons are mainly involved, the perception is typically tingling; if small-diameter axons are involved, it is commonly pain.
- Paresthesia - the same quality of abnormal sensation but occurring spontaneously, without any stimulus.
- Allodynia - pain perceived from a normally nonpainful stimulus (e.g., light touch).
- Hyperalgesia - excess pain from a mildly painful stimulus.
(Bradley and Daroff's Neurology in Clinical Practice, p. 534)
Pathophysiology
Paresthesia arises from aberrant electrical discharge of sensory nerve fibers. The key mechanisms are:
- Lowering of axonal membrane potential - minor deformation of a damaged nerve produces repetitive action potentials.
- Unstable membrane potential - fluctuation crests generate spontaneous action potentials.
- Ephaptic transmission (crosstalk) - an action potential in one damaged nerve fiber is abnormally transmitted to an adjacent fiber.
In demyelinating neuropathies, paresthesia tends to be the earliest feature. In axonal neuropathies, numbness and loss of pain/temperature sensation predominate.
Localization of Paresthesia
The distribution of paresthesia is the key diagnostic clue:
| Level of Lesion | Features |
|---|---|
| Cortical | Contralateral sensory loss restricted to the portion of the homunculus affected |
| Internal capsule | Contralateral head, arm, and leg equally affected; motor findings common |
| Thalamus | Contralateral body including head; sensory dysfunction without weakness is highly suggestive |
| Spinal transection | Sensory loss at or below a segmental level |
| Spinal hemisection (Brown-Séquard) | Ipsilateral vibration/proprioception loss; contralateral pain/temperature loss |
| Nerve root (radiculopathy) | Dermatomal distribution |
| Plexus | Spans two or more adjacent root distributions |
| Peripheral nerve | Follows peripheral nerve anatomy, or symmetric (polyneuropathy) |
(Bradley and Daroff's Neurology in Clinical Practice, Table 31.1)
Key localizing clues (peripheral):
- Distal sensory loss/pain in more than one limb → polyneuropathy
- Sensory loss in a restricted portion of one limb → mononeuropathy or plexopathy
- Sensory loss affecting an entire limb → rarely peripheral; seek a central lesion
Polyneuropathy Pattern ("Glove-and-Stocking")
Most polyneuropathies are length-dependent - the longest, largest axons are most affected first. Sensory loss begins distally in the feet and legs, and ascends proximally as the neuropathy progresses. The transition from normal to impaired sensation is gradual (a sharp border suggests psychogenic sensory loss).
(Adams and Victor's Principles of Neurology, 12th ed., p. 179)
Common Causes
Peripheral Causes
| Category | Examples |
|---|---|
| Metabolic/Endocrine | Diabetes mellitus (most common), hypothyroidism, hypo/hypercalcemia |
| Nutritional deficiency | Vitamin B12, B1 (thiamine - beriberi), B6 (pyridoxine), folate |
| Toxic/Drugs | Isoniazid (INH), chemotherapy, alcohol, thallium, aconite poisoning |
| Inflammatory/Autoimmune | Guillain-Barré syndrome, CIDP, vasculitic neuropathy, Sjögren syndrome |
| Infectious | Leprosy (sensory loss without paresthesia is characteristic; loss of pain/touch precedes paresthesia), HIV, Lyme disease |
| Compressive | Carpal tunnel syndrome (median nerve - nocturnal tingling, positive Tinel sign), disc herniation (dermatomal) |
| Hereditary | Charcot-Marie-Tooth disease |
Central Causes
| Category | Examples |
|---|---|
| Demyelinating | Multiple sclerosis (numbness, "pins and needles," coldness) |
| Vascular | Stroke/TIA (thalamic or cortical lesion) |
| Structural | Spinal cord compression, syringomyelia |
| Metabolic | Hypocalcemia (circumoral + peripheral tingling, carpopedal spasm, Chvostek/Trousseau signs) |
Fiber Type Involvement
| Fiber Type | Affected Modalities | Pattern |
|---|---|---|
| Large myelinated (Aα/Aβ) | Vibration, proprioception, fine touch | Sensory ataxia, pseudoathetosis; paresthesia is tingling |
| Small myelinated/unmyelinated (Aδ/C) | Pain, temperature, autonomic | Burning pain, trophic ulcers, Charcot joints; "pseudosyringomyelia" pattern |
Clinical Approach
- History - onset, distribution, quality (burning vs. tingling vs. numbness), progression (ascending vs. static), triggers, associated weakness/ataxia, systemic symptoms, medications, alcohol use, family history.
- Examination - map the sensory deficit carefully; test all modalities (pain, temperature, vibration, proprioception, light touch); check reflexes and power; look for autonomic features.
- Investigations guided by suspected etiology:
- Blood: glucose (HbA1c), B12, folate, B1, TSH, calcium, renal/hepatic function, ESR/CRP, SPEP, ANA, anti-dsDNA, anti-Ro/La
- EMG/Nerve conduction studies - distinguish axonal vs. demyelinating, mononeuropathy vs. polyneuropathy
- MRI brain/spine - for central causes
- Skin biopsy (intraepidermal nerve fiber density) - for small fiber neuropathy
- CSF analysis - for inflammatory/infective causes
Sources:
- Bradley and Daroff's Neurology in Clinical Practice, pp. 534-535 (Sensory Abnormalities, Table 31.1, Table 31.2)
- Adams and Victor's Principles of Neurology, 12th ed., p. 179 (Polyneuropathy)
- Rheumatology, 2-Volume Set (Peripheral Nervous System)
- Rosen's Emergency Medicine, Table 91.1 (MS clinical features)
- Harrison's Principles of Internal Medicine, 22nd ed. (Diabetic neuropathy, Thiamine deficiency)
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