Differential Diagnosis for Progressive Generalized Weakness with Nape Pain and Near-Syncope

This 35-year-old male requires immediate emergency evaluation for life-threatening neurological and cardiovascular emergencies, with subarachnoid hemorrhage, meningitis, Guillain-Barré syndrome, and cardiac syncope as the most critical considerations that cannot be dismissed. 1

The combination of progressive headache over 3 days with nape pain (neck stiffness) and near-syncope represents classic red flags for SAH that mandate immediate neuroimaging. 1
Sentinel headaches occur in up to 43% of patients 2-8 weeks before major aneurysm rupture, and posterior headache with neck stiffness cannot be dismissed even without the classic "thunderclap" presentation. 1
The feeling of losing consciousness may represent transient cerebral hypoperfusion from elevated intracranial pressure. 1
Non-contrast head CT must be obtained immediately (98-100% sensitivity in first 12 hours), followed by lumbar puncture if CT negative but clinical suspicion remains high. 1
Dismissing neck stiffness without neuroimaging leads to missed SAH in up to 12% of misdiagnosed cases. 1

Meningitis remains possible without fever, with neck stiffness (nape pain) being a key red flag that cannot be dismissed. 1
The absence of fever does not exclude bacterial meningitis, and CSF analysis remains the principal diagnostic contributor. 1
Progressive weakness and altered consciousness (near-syncope) can indicate evolving meningeal inflammation or encephalitis. 1
If CT is negative, lumbar puncture must be performed to evaluate for infection with cell count, protein, glucose, gram stain, culture, and xanthochromia. 1

GBS should be considered in any patient with rapidly progressive bilateral weakness, particularly when accompanied by numbness and dysautonomia (near-syncope). 1
Disease onset is typically acute or subacute, with patients reaching maximum disability within 2 weeks. 1
Dysautonomia is common and includes blood pressure or heart rate instability that can manifest as near-syncope. 1
Pain is frequently reported and can be muscular, radicular, or neuropathic, potentially explaining the nape pain. 1
Reflexes are decreased or absent in most patients at presentation—this must be assessed on examination. 1

The feeling of losing consciousness represents presyncope, and cardiac causes of syncope carry the highest mortality risk and must be excluded. 1, 2
Progressive generalized weakness may indicate reduced cardiac output from arrhythmia, structural heart disease, or mechanical obstruction. 1
All patients with presyncope require electrocardiography as initial evaluation. 1
Arrhythmic causes include sinus node dysfunction, atrioventricular conduction disease, paroxysmal supraventricular and ventricular tachycardias, and inherited syndromes such as Long QT syndrome and Brugada syndrome. 2
Structural cardiac causes include acute myocardial infarction/ischemia, obstructive valvular disease, acute aortic dissection, and pulmonary embolus. 2

CVT can present with prolonged headache (weeks to months) followed by acute focal neurological deficits, making this a critical consideration. 3
Typical signs on MRI include signal loss of the affected cortical vein in T2-susceptibility-weighted sequences and ipsilateral dural thickening and enhancement. 4
The mean time between symptom appearance and diagnosis is 7 days, and headache with neck pain can be the presenting features. 4
CT venography or MR venography is required if there is any suspicion for CVT, as standard CT may miss this diagnosis. 3

Progressive weakness lasting three days strongly suggests ischemic stroke, as these symptoms persist longer than 24 hours by definition. 3
The preceding headache may represent warning TIAs or evolving vascular pathology. 3
Non-contrast head CT is the first-line imaging study in the acute setting, followed by CT angiography to assess both extracranial and intracranial circulation. 3

SIH can present with severe headache worsened by upright position, neck pain, and if not recognized early, results in complications including subdural hematoma. 5
Any change in headache pattern in SIH must alert the clinician to possible complications. 5

Stabilize airway, breathing, circulation per ABCDE protocol, and obtain vital signs including orthostatic measurements (drop in systolic BP ≥20 mmHg or diastolic BP ≥10 mmHg suggests orthostatic hypotension). 1
Perform focused neurological examination looking for:
- Meningismus/nuchal rigidity (neck stiffness) 1
- Focal neurological deficits 1
- Reflex abnormalities (decreased/absent suggests GBS) 1

Non-contrast head CT immediately to exclude SAH, mass lesion, or acute stroke. 1, 3
Electrocardiogram to exclude cardiac arrhythmia or ischemia. 1
If CT negative but neck stiffness present: lumbar puncture for cell count, protein, glucose, gram stain, culture, and xanthochromia. 1
If CVT suspected: CT venography or MR venography. 3

Patients with suspected cardiac syncope, unexplained syncope after initial evaluation, or features suggesting serious conditions require specialist cardiovascular or neurological assessment. 1
Immediate neurosurgical consultation if SAH confirmed. 1
Admit for monitoring and further workup if GBS suspected (intravenous immunoglobulin 0.4 g/kg daily for 5 days or plasma exchange). 1

Assuming absence of fever rules out meningitis is incorrect, as clinical characteristics have limited diagnostic accuracy. 1
Failing to recognize presyncope as a warning sign of impending complete syncope from cardiac causes. 1
Overlooking the progressive nature of symptoms over 3 days as a red flag for secondary pathology. 1
Attributing progressive weakness to benign causes without excluding GBS can delay life-saving treatment, particularly if respiratory muscle involvement develops. 1
Delaying neuroimaging in any patient with new neurological deficits, regardless of headache characteristics. 3