Neuroanatomy & Tracts

The three long tracts

Dorsal columns (medial lemniscus). Carry fine touch, vibration, and proprioception. First-order fibers from the dorsal root ganglion ascend ipsilaterally: fasciculus gracilis (legs) medially and fasciculus cuneatus (arms) laterally. They synapse in the nucleus gracilis and cuneatus of the caudal medulla, where second-order neurons decussate as internal arcuate fibers and ascend as the medial lemniscus to the thalamus (VPL). A lesion anywhere below the medulla therefore gives ipsilateral loss.

Gracilis is graceful and medial, for the legs; the arms are added laterally in cuneatus.

Spinothalamic tract. Carries pain and temperature (and crude touch). First-order neurons synapse in the dorsal horn; second-order neurons decussate in the anterior white commissure within 1–2 levels of entry and ascend on the opposite side to the thalamus. A cord lesion therefore causes contralateral pain and temperature loss beginning a couple of levels below it.

Lateral corticospinal tract. Carries voluntary motor commands. Upper motor neurons (UMNs) descend from the motor cortex through the internal capsule and brainstem, decussate at the pyramidal decussation in the caudal medulla, and synapse on lower motor neurons (LMNs) in the anterior horn. UMN lesions cause spasticity, hyperreflexia, and a Babinski sign; LMN lesions cause flaccidity, atrophy, fasciculations, and areflexia.

Classic spinal cord lesions

Brown-Séquard syndrome (cord hemisection). Below the lesion: ipsilateral loss of motor function (corticospinal) and vibration/proprioception (dorsal columns), plus contralateral loss of pain and temperature (spinothalamic) starting about 2 levels down. At the level: ipsilateral LMN flaccid paralysis. A high lesion (above T1) adds ipsilateral Horner syndrome.

Syringomyelia. A central cord cavity (syrinx) first destroys the spinothalamic fibers crossing in the anterior white commissure, producing bilateral pain and temperature loss in a cape distribution (C8–T1) with preserved touch and vibration: dissociated sensory loss. It is associated with Chiari I malformation; expansion into the anterior horns adds LMN signs in the hands.

Subacute combined degeneration. Vitamin B12 deficiency demyelinates three tracts: the dorsal columns (loss of vibration and proprioception, positive Romberg), the lateral corticospinal tracts (spastic paresis, Babinski), and the spinocerebellar tracts (ataxia). Vitamin E deficiency produces a similar picture, and Friedreich ataxia hits the same tracts in a young patient. Folate can correct the macrocytic anemia of B12 deficiency but not the cord damage.

Tabes dorsalis. Tertiary syphilis degenerates the dorsal columns and dorsal roots: impaired proprioception, sensory ataxia, positive Romberg, Charcot joints, shooting pains, and Argyll Robertson pupils, which accommodate but do not react to light.

Amyotrophic lateral sclerosis. Destroys both upper and lower motor neurons (corticospinal tract plus anterior horn) with no sensory loss. SOD1 mutations cause some familial cases, and riluzole (which reduces glutamate release) extends survival.

Cerebellum and basal ganglia

Cerebellum. Lesions cause ipsilateral deficits because the pathways cross twice and the crossings cancel out. Lateral hemisphere lesions cause limb dysmetria, intention tremor, dysdiadochokinesia, and falling toward the side of the lesion. Vermis/midline (flocculonodular) lesions cause truncal ataxia, a wide-based gait, and nystagmus. Purkinje cells, the only output of the cerebellar cortex, are inhibitory; the deep nuclei, chiefly the dentate, send output through the superior cerebellar peduncle.

Basal ganglia. The direct pathway (D1, excitatory) facilitates movement by disinhibiting the thalamus; the indirect pathway (D2, inhibitory) suppresses movement through the subthalamic nucleus, which drives the inhibitory output nuclei. Dopamine from the substantia nigra pars compacta (SNc) stimulates D1 and inhibits D2, a net push toward movement.

• Parkinson disease: loss of SNc dopamine → hypokinetic disorder.
• Huntington disease: loss of GABAergic caudate neurons → hyperkinetic chorea.
• Subthalamic nucleus lesion (often a lacunar stroke) → contralateral hemiballismus, with wild flinging movements.

Hypothalamus and brainstem

Hypothalamic functions. TAN HATS: Thirst, Adenohypophysis control, Neurohypophysis, Hunger, Autonomic, Temperature, Sexual urges.

• Lateral nucleus: hunger; lesion causes anorexia.
• Ventromedial nucleus: satiety; lesion causes hyperphagia and obesity. Leptin stimulates this nucleus and inhibits the lateral one.
• Anterior: cooling and parasympathetic (A/C), although sweating, the main heat-loss effector, is sympathetic cholinergic; posterior: heating and sympathetic.
• Supraoptic makes ADH and paraventricular makes oxytocin, both released from the posterior pituitary.
• Suprachiasmatic: sets circadian rhythm.

Zap the Lateral nucleus and you Lose weight; zap the ventroMedial nucleus and you become Massive.

Cranial nerves by level. The midbrain holds CN III and IV; the pons holds V, VI, VII, and VIII; the medulla holds IX, X, and XII. CN IV is the only nerve that exits dorsally, and it decussates. Motor nuclei lie medially (III, IV, VI, XII).

• Pupillary light reflex: II in, III out.
• Corneal reflex: V1 in, VII out.
• Gag reflex: IX in, X out.
• Jaw jerk: V in and out.
• CN X mediates the cough reflex and most parasympathetic supply to the viscera.

Cerebral arteries and stroke syndromes

Anterior circulation. The ACA supplies the medial frontal and parietal cortex, where the leg is represented, so ACA stroke causes contralateral leg weakness and sensory loss. The MCA supplies the lateral convexity, producing contralateral face and arm deficits plus aphasia in the dominant hemisphere (Broca: nonfluent speech with intact comprehension; Wernicke: fluent speech with poor comprehension) or hemineglect in the nondominant hemisphere.

Posterior circulation. PCA stroke infarcts occipital cortex, causing contralateral homonymous hemianopia with macular sparing. PICA occlusion causes the lateral medullary (Wallenberg) syndrome: ipsilateral facial pain/temperature loss, contralateral body pain/temperature loss, dysphagia and hoarseness, vertigo, and ipsilateral Horner syndrome.