How can I localize central nervous system (CNS) symptoms in an adult with no prior neurological disease?

Localizing Central Nervous System Symptoms

To localize CNS symptoms, systematically map the clinical findings to specific anatomical structures by determining whether the pathology affects the brain parenchyma, brainstem nuclei, cranial nerve pathways from nucleus to end organ, spinal cord, or vascular territories—using the principle that lesions produce symptoms corresponding to the specific neural structures they damage. 1

Fundamental Localization Principles

Key Anatomical Concepts

• Pathology can affect nerve fibers at any point from the CN nucleus to the end organ, and processes affecting brain, CN nuclei, or nerve fiber tracts are typically associated with multiple neurologic symptoms rather than isolated findings. 1

• Individual nerve fibers (particularly autonomic nerves) may travel with several different cranial nerves from their nuclei of origin to ultimate destinations, so loss of a specific function may indicate involvement of more than one cranial nerve. 1

• The close proximity of many CN nuclei, CN segments, and exiting sites means some lesions produce multiple cranial neuropathies simultaneously. 1

• Lesions must be at least 3 mm in the largest linear measurement in at least one plane to be considered clinically significant on imaging. 1

Systematic Localization Algorithm

Step 1: Determine Level of Involvement

• Cortical/hemispheric lesions produce contralateral motor or sensory deficits, language dysfunction (if dominant hemisphere), visual field cuts, or seizures. 2, 3

• Brainstem lesions typically cause ipsilateral cranial nerve deficits combined with contralateral long tract signs (crossed findings), plus associated symptoms like nystagmus, vertigo, ataxia, nausea, and vomiting. 1

• Spinal cord lesions produce bilateral motor/sensory deficits below the level of the lesion, with a sensory level on examination. 1

• Peripheral nerve lesions cause deficits in the distribution of specific nerves without central signs. 2

Step 2: Identify Vascular Territory (If Ischemic)

• Carotid territory symptoms include contralateral hemiparesis, hemisensory loss, aphasia (dominant hemisphere), or neglect (non-dominant hemisphere). 3

• Vertebrobasilar territory symptoms include bilateral motor/sensory deficits, crossed brainstem findings, ataxia, vertigo, diplopia, dysarthria, or dysphagia. 4

• Posterior circulation strokes can mimic peripheral vestibular processes in 10% of cases and are frequently missed on CT imaging—MRI with diffusion-weighted imaging is required. 2

Step 3: Localize Cranial Nerve Involvement

• CN I-II originate from telencephalon and diencephalon respectively and are not true nerves; dysfunction suggests anterior brain pathology. 1

• CN III-IV-VI nuclei are in the midbrain and pons; lesions cause diplopia and pupillary abnormalities with specific patterns based on which nerve is affected. 1

• CN V nucleus is in the pons; lesions cause facial sensory loss and/or masticatory weakness in trigeminal distribution. 1

• CN VII nucleus is in the pons; lesions cause ipsilateral facial weakness including forehead (distinguishing it from cortical lesions which spare forehead). 1

• CN IX-X-XI nuclei are in the medulla; lesions cause dysphagia, dysphonia, loss of gag reflex, and shoulder/neck weakness. 1

• CN XII nucleus is in the medulla; lesions cause tongue deviation toward the side of the lesion. 1

Step 4: Recognize Specific Brainstem Syndromes

• Lateral medullary syndrome (Wallenberg) from posterior inferior cerebellar artery occlusion causes ipsilateral facial sensory loss, Horner syndrome, ataxia, and contralateral body sensory loss. 1

• Jugular foramen syndromes produce variable patterns: Vernet syndrome (CN IX, X, XI), Collet-Sicard syndrome (CN IX, X, XI, XII), and Villaret syndrome (CN IX, X, XI, XII plus cervical sympathetic trunk). 1

• Multiple lower cranial nerve palsies suggest lesions at the jugular foramen (paragangliomas, schwannomas, meningiomas), leptomeningeal processes, or internal carotid dissection. 1

Critical Diagnostic Pitfalls

Common Localization Errors

• Bilateral numbness with headache or altered mental status suggests increased intracranial pressure, meningitis, or stroke requiring urgent neuroimaging—do not attribute to peripheral causes. 2

• Purely sensory symptoms (numbness, pain, paresthesia) require consideration of radiculopathy, neuropathy, microvascular cerebral/spinal pathology, or lacunar stroke—not just peripheral nerve disease. 1

• Nonfocal neurological events (transient global amnesia, acute confusion, syncope, isolated vertigo, nonrotational dizziness) have uncertain relationship to cerebrovascular disease and require broader differential diagnosis. 1

• Brief, stereotyped, repetitive symptoms suggest partial seizure rather than TIA—electroencephalography is indicated. 1

High-Risk Scenarios Requiring Urgent Evaluation

• Sudden-onset numbness with focal deficits suggests acute stroke, though up to 80% of posterior circulation strokes may lack obvious focal findings. 2

• Scalp tenderness, jaw claudication (positive likelihood ratio 4.90), or temporal headache in patients over 50 years demands immediate ESR and CRP for giant cell arteritis—never delay corticosteroids while awaiting results if vision symptoms present. 2

• Acute onset with rapid progression of bilateral numbness and weakness requires lumbar puncture and nerve conduction studies to rule out Guillain-Barré syndrome. 2

• Intermittent dizziness with high-grade vertebral artery stenosis (especially V4 segment) requires emergency evaluation due to high stroke risk—up to 13% in first 90 days. 4

Essential Imaging Approach

MRI Protocol Selection

• MRI is the standard modality for imaging cranial nerves and CNS pathology; 3.0T is preferred over 1.5T for superior signal-to-noise ratios, gradient strength, and spatial resolution. 1

• Fundamental sequences include thin-cut T1-weighted, T2-weighted, and contrast-enhanced T1-weighted imaging—intravenous contrast is imperative for evaluating cranial neuropathy. 1

• Diffusion-weighted imaging is useful to assess acute infarctions, cellular tumors, epidermoids, or cholesteatomas. 1

• Complete evaluation requires imaging from brainstem nuclei to end organs: for CN VII include parotid; for CN IX-XII include neck; for CN X include upper chest to aortic-pulmonary window for recurrent laryngeal nerve. 1

When to Use CT

• CT with thin-cut high-resolution bone algorithm windows is complementary to MRI for delineating skull base fractures, hyperostosis, skull base erosion, or intratumoral calcification. 1

• CT frequently misses posterior circulation strokes—MRI with diffusion-weighted imaging is required for definitive diagnosis. 2

Workup for Multiple Cranial Neuropathies

• In patients with multiple cranial neuropathies, imaging is useful to exclude intraparenchymal processes, but addition of cerebrospinal fluid analysis and serologic studies may be indicated for extraparenchymal causes. 1

• Leptomeningeal processes can lead to variable patterns of cranial neuropathy and require lumbar puncture for diagnosis. 1

• Internal carotid artery dissection can result in isolated acute CN XII palsy or less commonly multiple variable patterns of CN palsies including CN IX-XII. 1