An approach to…

Neurologic Localization

Updated September 2025 by Dr. Dan Berger

Levels of the nervous system

Thalamus

Basal ganglia

Cortex

Corona radiata/internal capsule

Brainstem

Spinal cord

Anterior horn cell (LMN cell body)

Spinal nerve roots

Plexus

Peripheral nerve

Muscle

Additional unique localizations:

Cerebellum

Upper and lower motor neuron

Upper motor neuron

Lower motor neuron

Upper motor neuron

Lower motor neuron

Function

Weakness

Reflexes

Tone

Muscle mass

Fasciculations

Plantars

Inhibitory effect on muscle stretch reflex

Motor component of muscle reflex

Pyramidal weakness

Myotomal/plexus/peripheral nerve pattern weakness

Brisk or hyper-reflexic

Normal or reduced reflexes

Spastic

Normal or hypotonic

Normal, or disuse-type atrophy

Significant wasting-type atrophy

Present

None

Upgoing

Downgoing

Hint: look for the presence of multiple features – i.e., don’t rely on only hyperreflexia, look for a combination of features to help you localize a lesion as UMN or LMN. Then, refine your localization from there!

Cortex

• Aphasia (frontal and temporal lobe)
• Fluent + can’t comprehend + can’t repeat → Wernicke’s receptive aphasia (superior temporal gyrus)
• Non-fluent + can comprehend + can’t repeat → Broca’s productive aphasia (inferior frontal gyrus)

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• Parietal lobe
• Apraxia (inability to carry out learned motor tasks)
• Acalculia (inability to do math)
• Finger agnosia (can’t recognize fingers)
• Agraphesthesia (can’t recognize numbers/letters traced on hand)
• Astereognosis (can’t recognize objects by touch)
• Hemineglect
• Alexia (inability to read)
• Agraphia (inability to write)

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• Occipital lobe
• Homonymous hemianopia

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Hint: remember to screen for delirium (attentional task, look for fluctuations) to separate true cortical findings from delirium.

Corona radiata/internal capsule

• Corona radiata (subcortical) is more loosely packed white matter tracts, produces patchy/incomplete sensorimotor deficits (face > arm or arm > leg).
• Internal capsule is densely packed – lesions often produces face = arm = leg weakness/sensory loss.

• Lacunar syndromes: Lacunar meaning “small lake” (typically <2 cm), infarcts in the deep brain or brainstem usually from small vessel disease. None have cortical findings.
• Pure motor: contralateral face=arm=leg weakness, posterior limb of the internal capsule or pons.
• Pure sensory: contralateral face=arm=leg sensory loss (all modalities), ventral posterolateral/medial thalamic nucleus.
• Sensorimotor: contralateral weakness/sensory loss, thalamocapsular junction (a mix of the two above)
• Ataxic hemiparesis: contralateral mild weakness and limb ataxia, corona radiata/internal capsule/pons.
• Dysarthria-clumsy hand: dysarthria, facial weakness, weakness/clumsiness of the contralateral hand, genu of the internal capsule (corticobulbar tract) or pons.

Hint: the key with subcortical localizations (except thalamic) is typically the absence of cortical findings (no aphasia/apraxia etc) and the presence of hemi-body sensorimotor deficits.

Thalamic localization

Unique localization, multiple nuclei/regions that do different things. Think about it with:

• Pure sensory (VPL/VPM nuclei),
• “Thalamic hand”/involuntary movements/asterixis
• Presentations with confusion, amnesia, somnolence, apathy (medial thalamus
• Milder aphasias (typically dominant thalamus).

Internal capsule anatomy

• Posterior limb: corticospinal motor and thalamocortical sensory fibers
• Genu: corticobulbar tract (facial strength)
• Anterior limb: frontal-pontine fibers, anterior thalamic radiations (thalamus, frontal lobe, limbic circuitry)

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Brainstem

Hint: for brainstem, look for cranial nerve findings, and crossed findings (cranial nerve lesions ipsilateral, motor/sensory deficits contralateral).

• General principles
• Cranial nerve nuclei (III-XII) all in the brainstem, help you localize to a specific level.
• Long tracts (corticospinal, spinothalamic, dorsal columns) run through all segments.
• Cerebellar connections traverse multiple segments.

• Midbrain
• CN III (oculomotor) and CN IV (trochlear) nuclei

Brainstem “Rule of 4”

• 4 pathways that are “midline” in the brainstem that start with “M”
• 4 pathways that are lateral (“sideways”) that start with “S”
• 4 cranial nerves that divide into 12 that are midline (3, 4, 6, 12)

• Pons
• CN V (trigeminal), VI (abducens), VII (facial) and VIII (vestibulocochlear) nuclei

• Medulla
• CN IX (glossopharyngeal), X (vagus), XI (spinal accessory) and XII (hypoglossal) nuclei

Side (lateral) tracts:

1. Sympathetic pathway
2. Spinothalamic tract
3. Spinocerebellar
4. Sensory nucleus (CN V)

Midline tracts:

1. Motor nucleus (trigeminal)
2. Motor pathway (corticospinal)
3. Medial lemniscus
4. Medial longitudinal fasciculus

Hint: remember the reticular activating system is in the brainstem! Brainstem can be a rare localization for encephalitis too (often infectious, autoimmune, paraneoplastic)

Spinal cord

Hint: if you’re thinking about a spinal cord process, as about Lhermitte’s and Uhthoff’s phenomenon and radicular pain to start narrowing down your differential a bit more.

• General principles
• Bilateral motor/sensory and often autonomic deficits (not hemi-body deficits like a cerebral localization), below the level of the lesion.
• Bowel and bladder involvement is a strong clue for spinal cord localization.
• A spinal sensory level (test with pinprick, confirm with temperature!) suggests a spinal cord localization.

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Corticospinal tracts (organized somatotopically with face/arm more medial) decussate in the medulla

Dorsal columns

(organized somatotopically with legs more medial) decussate in the medulla

Spinothalamic tract

Decussate in the spinal cord, 1-3 levels below the lesion

Sympathetic fibers

Thoracolumbar outflow from the anterior horn (grey matter)

• Spinal “syndromes”
• Hemicord syndrome: ipsilateral UMN features and vibration/proprioception deficits, contralateral pain/temperature deficits.
• Central cord syndrome: cape-like pain/temperature loss, UE weakness > LE weakness
• Anterior cord syndrome: loss of motor, pain/temperature below lesion, but preservation of vibration/proprioception.
• Posterior cord syndrome: loss of vibration/proprioception below lesion, sensory ataxia, + Romberg.

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Anterior horn cell

• Anterior horn cells
• Cell body of the “lower motor neuron” is in the anterior horn of the spinal cord.
• Localization will be motor only, no sensory involvement (typically no pain).
• LMN features usually confined to level of lesion with weakness in a myotomal pattern, significant atrophy, fasciculations, and hyporeflexia/areflexia (though finding all of these usually only happens in later stages of disease).
• Pure anterior horn cell disorders are things like spinal muscular atrophy, poliomyelitis, and Hirayama disease (monomelic amyotrophy).

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• Amyotrophic lateral sclerosis
• Unique localization in neurology with LMN signs (which happen as the anterior horn cells are damaged/die off) and UMN signs (which happen as the corticospinal and corticobulbar tracts are damaged).
• Will see atrophy, fasciculations, but also spasticity, brisk reflexes (particularly concerning when they’re in wasted muscles).
• The LMN signs dominate at the site of earliest involvement, and typically spreads via contiguous myotomal progression.
• Special clinical signs to “level up” your localization include a split hand sign (preferential wasting of the thenar + FDI vs the hypothenar muscles), tongue fasciculations/atrophy, paraspinal muscle atrophy, brisk jaw jerk.

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Anterior horn cell

Spinal nerve roots

• Spinal nerve roots
• 31 pairs, each corresponding to a dermatomal sensory distribution and myotomal motor distribution.
• In the cervical spine,
• LMN findings include sensory deficits, pain, paresthesias along a dermatome, mild motor weakness in a myotomal distribution, normal or reduced reflexes, and occasionally atrophy, fasciculations.
• Common etiologies include compressive/spondylotic radiculopathies, or acute/chronic demyelinating polyradiculoneuropathies (Guillain-Barré syndrome).
• Spinal cord ends around L1, and the cauda equina (bundle of nerve roots from L2-S5) descends from there. Conus medullaris lesions often present with UMN features, but compression of the cauda equina produces LMN signs, with numbness/tingling in the saddle distribution, bowel and bladder dysfunction, sexual dysfunction, leg pain and motor weakness in the legs.

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Mixed spinal nerve

Sensory root (dorsal)

Dorsal root ganglion

Motor root (ventral)

Hint: remember, dermatomes have ill-defined borders, and most muscles have multiple spinal levels innervating them. Radicular sensory findings are usually fuzzy/incomplete, and motor weakness is mild.

Disc herniation and resulting radiculopathy (most often the mixed spinal nerve affected)

Plexus

Hint: here is a link to my favorite brachial plexus diagram (which includes all of the smaller nerves) https://geekymedics.com/brachial-plexus/

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Median nerve

Axillary nerve

Musculocutaneous nerve

Radial nerve

Ulnar nerve

Posterior cord

Medial cord

Lateral cord

• When we say “plexus”, we’re typically talking about the brachial plexus (motor and sensory information from C8 to T1) or the lumbosacral plexus (motor and sensory information from T12/L1 to S4) .
• Plexus localizations usually involve “chaos” in a limb, affecting multiple nerves and roots, producing a confusing pattern of patchy sensory and motor involvement (typically motor > sensory involvement).
• Exclusively LMN findings including weakness, atrophy, fasciculations, normal-to-reduced reflexes.

• Etiologies include:
• Brachial neuritis: idiopathic, vaccine/viral-related, post-surgery. Typically heralded by significant clavicular/shoulder/upper arm pain, preferentially involves the upper trunk (affects shoulder abduction, external rotation, biceps most).
• Diabetic lumbosacral radiculoplexus neuropathy (“diabetic amyotrophy”) is an immune-mediated microvasculitis, again heralded by hip/thigh/buttock pain, then weakness/sensory symptoms proximal first, then typically distal later.
• Others like traction injuries (trauma, post-surgery), birth trauma (Erb’s palsy),inflammatory/immune-mediated, malignant infiltration, many more. radiation-induced,

Peripheral nerve

• Peripheral nerves typically carry motor (somatic efferent) and sensory (somatic afferent) information, as well as other divisions like parasympathetic/sympathetic or special senses (things like taste with the facial nerve, special somatic afferent).
• Injury to peripheral nerves produces LMN motor features, and typically sharply demarcated sensory deficits (in contrast to the fuzzy boundaries of a dermatome).
• Deficits follow the territories of a specific nerve, which gets more complex the more proximal the lesion is (i.e. as it innervates more muscles and broader areas of sensation).
• Physical examination features can help – things like a “claw hand” or “sign of Benediction” or “pes cavus” can point you towards a peripheral nerve lesion at a specific localization.
• Typical patterns we think of:

Median nerve digital branches

Palmar ulnar cutaneous

Dorsal ulnar cutaneous

Ulnar nerve digital branches

Superficial radial

Ulnar nerve

Median nerve

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• Distal symmetric polyneuropathy – “stocking glove” typically involving sensory first, then motor, worse distally, and then proximally.
• Mononeuropathy – entrapment mononeuropathies like median or ulnar are common!
• Multifocal neuropathies – concerning for an inflammatory neuropathy like vasculitis.
• Autonomic neuropathies – come with a host of autonomic symptoms (orthostatic intolerance, sexual dysfunction, dysphagia etc).

Neuromuscular junction

• The neuromuscular junction (NMJ) is a unique localization in neurology.
• Hallmark feature is fatigable weakness – there are no sensory findings in this localization, and tone, reflexes and muscle bulk are most often normal.
• Hints for localization will be a story of fluctuating motor weakness (proximal > distal), fluctuating ptosis/dysarthria/diplopia/dysphagia.
• Prototypical diseases are:
• Myasthenia gravis: autoimmune destruction of (most typically) the nicotinic acetylcholine receptor (AChR), though other proteins involved are MuSK and LRP4 (both at the NMJ). No autonomic features, sensory symptoms, or pain.

Muscle contraction

ACh release and binding to AChR

• Lambert-Eaton myasthenic syndrome: autoimmune destruction of the presynaptic voltage-gated calcium channels that reduces ACh release. Presents with proximal > distal weakness usually legs > arms, autonomic symptoms, and hyporeflexia/areflexia at rest (reflexes can improve in the 1-2 seconds following brief exercise).

Muscle

• This localization is tough! Problems are inherent in the muscle itself, not the nervous system.
• Clues on history and physical examination are pattern of weakness (proximal > distal suspicious for myopathy), symmetric weakness, myalgia, cramps, fatigue, reduced exercise tolerance, systemic features like rash, fatigue, weight loss.
• Can have ocular/bulbar symptoms like ptosis, diplopia, dysphagia, facial weakness.
• No sensory symptoms (unless a secondary neuropathy is present).
• Will see muscle wasting/atrophy over time, or pseudohypertrophy (like in Duchenne muscular dystrophy) but typically no fasciculations (differentiates from a nerve problem).
• Differential is broad, and largely guided by pattern of weakness.
• Inherited: muscular dystrophies like Duchenne, Becker muscular dystrophy (see below), mitochondrial (MELAS, MERRF), metabolic (McArdle’s, Pompe disease).

• Acquired: inflammatory like dermatomyositis, polymyositis, inclusion body myositis, endocrine like thyroid myopathy, toxic like statin (immune mediated necrotizing myositis), critical illness myopathy, and many more.

Weakness patterns in inherited muscular dystrophies

a) Duchenne and Becker MD, b) Emery-Dreifuss MD, c) Limb-girdle MD, d) Facioscapulo-humeral MD, e) distal MD, f) oculopharyngeal MD

Cerebellum

• Three functional divisions:
• Vestibulocerebellum: flocculonodular lobe, coordinates balance, posture, eye movements. Lesions produce truncal ataxia (unsteady, wide-based gait), postural instability (can’t sit upright without support), vertigo/nausea/vomiting, nystagmus/impaired saccades.
• Spinocerebellum: vermis and intermediate hemispheres, manages trunk and limb coordination, axial muscle tone. Lesions produce truncal instability, wide based gait, and limb ataxia/dysmetria (finger-nose and heel-shin issues).
• Cerebrocerebellum: lateral cerebellar hemispheres, manage skilled motor movements, motor learning. Presents with ipsilateral limb ataxia, intention tremor with distal movements, ataxic dysarthria (“scanning speech”), cognitive changes (cerebellar affect).

• Hints for localization include wide-based, unsteady gait and inability to tandem walk, intention tremor and dysmetria on finger-nose or heel-shin, irregular scanning-type speech, truncal/head titubation, impaired smooth pursuit, saccadic dysmetria, nystagmus, and mild hypotonia.

Hint: you need the integration of many systems for steady gait, including sensory (large fiber particularly), visual, vestibular, and cerebellar. Ataxic gait can localize to problems in any, or all of these. Think about how you would interrogate each system to understand more.

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Basal ganglia

• The basal ganglia are a set of deep grey matter nuclei involved in movement initiation and scaling, motor learning, and cognition/behaviour (via the limbic system).
• Basal ganglia localization produces movement disorders, rather than weakness or ataxia.
• Movement disorders can be hypokinetic – typically, the only one you’ll see is parkinsonism:
• Bradykinesia (slow, decrementing movements), rigidity (velocity independent tone), a rest tremor (typically 4-6 Hz), postural instability and hypomimia (masked facies).
• Localization is loss of dopaminergic neurons in the substantia nigra, and loss of dopamine output to the caudate and putamen (which eventually causes excessive inhibition on the thalamus and hypokinetic movements).

• The other movement disorders of the basal ganglia are the hyperkinetic ones:
• Chorea – irregular, unpredictable, non-stereotyped flowing movements, “dance-like”.
• Dystonia – sustained/intermittent muscle contractions causing abnormal, repetitive (stereotyped), patterned postures or twisting movements.
• Ballismus – large amplitude flailing movements, typically unilateral.
• Myoclonus – rapid, sudden, jerk-like movements, focal/multifocal or generalized.
• Tics – recurrent, stereotyped, rapid movements (motor) or sounds (phonic), suppressible (for a short time, until rebound), associated with a premonitory urge.
• Athetosis – slow, writhing, sinuous movements of the distal limbs, overlaps with chorea often.
• Akathisia – subjective inner sense of restlessness with observable motor manifestations.
• Tremor – rhythmic, oscillatory involuntary movement (can be postural, rest or kinetic).

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