MDM Templates

Paresthesia — Benign / Peripheral

Patient presents with tingling/numbness in a peripheral distribution. No motor deficits, no facial involvement, no speech changes. Normal neurologic exam including strength, gait, and coordination.

Distribution and exam consistent with peripheral etiology (mononeuropathy, entrapment, radiculopathy). Not consistent with stroke (no motor deficit, no facial involvement, no cortical signs), spinal cord pathology (no sensory level, no bilateral symptoms, no bladder dysfunction), or GBS (no ascending weakness, no areflexia).

Plan: Discharge with PCP follow-up for further evaluation. Return for weakness, facial droop, speech changes, difficulty walking, or worsening symptoms.

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Paresthesia — Stroke Concern

Patient presents with acute onset numbness with features concerning for central etiology — hemisensory distribution, associated motor weakness, facial involvement, or cortical signs (neglect, aphasia, visual field deficit).

Acute onset with central distribution pattern raises concern for stroke. Not consistent with peripheral neuropathy (hemisensory, not dermatomal), carpal tunnel or entrapment (distribution too broad, associated findings), or hyperventilation-related paresthesia (pattern and associated features inconsistent).

If neurology consulted: Neurology consulted regarding patient’s deficits, imaging, and disposition.

Plan: Stroke workup initiated. Admit.

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Clinical Education

Approach to Paresthesia in the ED

Most paresthesia in the ED is benign. The vast majority of patients presenting with isolated tingling/numbness have a peripheral cause (carpal tunnel, ulnar neuropathy, radiculopathy) or a benign systemic cause (hyperventilation, anxiety). The ED job is to identify the minority with dangerous causes and safely discharge the rest with appropriate follow-up.^[1]

The key question is distribution. A dermatomal pattern suggests radiculopathy. A single nerve territory suggests mononeuropathy or entrapment. A stocking-glove pattern suggests peripheral neuropathy. A hemisensory pattern or non-dermatomal distribution should raise concern for a central cause.

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Localization by Pattern

Pattern	Likely Cause	ED Action
Single nerve territory (median, ulnar, peroneal)	Entrapment neuropathy	Discharge with PCP/neurology follow-up
Dermatomal	Radiculopathy, herpes zoster (pre-rash)	Discharge unless motor deficit
Stocking-glove	Peripheral neuropathy (DM, B12, alcohol)	Check glucose, B12, discharge with follow-up
Hemisensory	Stroke (thalamic), MS	Stroke workup
Bilateral hands/feet + sensory level	Spinal cord pathology	MRI spine, neurology consult
Bilateral perioral + bilateral hands	Hyperventilation	Reassurance, treat underlying anxiety

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Dangerous Causes Not to Miss

Stroke: Acute hemisensory symptoms, especially with any motor component, facial involvement, or cortical signs. Pure sensory stroke (thalamic lacunar infarct) presents with numbness only and no motor deficit — easy to dismiss. If the onset was sudden and the distribution is hemisensory, get the workup.^[1]

Spinal cord compression: Bilateral symptoms, a sensory level, or any bladder/bowel dysfunction. Requires emergent MRI.

GBS: Ascending paresthesia followed by ascending weakness. The paresthesia often comes first by hours to days. If the patient describes tingling starting in the feet and moving up, check reflexes — areflexia with ascending symptoms is GBS until proven otherwise.

Cauda equina: Saddle anesthesia, urinary retention, bilateral leg symptoms. Emergent MRI.

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Disposition

Discharge: Isolated paresthesia in a peripheral distribution with normal neurologic exam and no red flags. Ensure follow-up for further evaluation (EMG/NCS, labs, outpatient imaging as needed).

Admit / urgent workup: Any hemisensory pattern (stroke workup), bilateral symptoms with sensory level (cord pathology), ascending paresthesia with weakness or areflexia (GBS concern), or saddle anesthesia with bladder dysfunction (cauda equina).

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References

1. Edlow JA, Selim MH. Atypical presentations of acute cerebrovascular syndromes. Lancet Neurol. 2011;10(6):550-560. PubMed