CNRN Exam

This chapter covers the cerebral lobes and deep structures, language and hemispheric dominance, the brainstem and cerebellum, the twelve cranial nerves and how to test them, the major spinal cord tracts, dermatomes and reflexes, upper versus lower motor neuron signs, and the autonomic nervous system.

The cerebrum is divided into right and left hemispheres, connected by the corpus callosum. Each hemisphere controls movement and sensation on the opposite side of the body because the major motor and sensory pathways cross.

Cerebral Lobes, Functions and Deficits

The primary motor cortex lies in the precentral gyrus of the frontal lobe and the primary sensory cortex in the postcentral gyrus of the parietal lobe. Both are arranged as a homunculus: the leg and foot are represented on the medial surface near the midline (anterior cerebral artery territory), while the face, arm and hand are on the lateral surface (middle cerebral artery territory). This map explains why an ACA stroke weakens the leg more than the arm, and an MCA stroke weakens the face and arm more than the leg.

The left hemisphere is dominant for language in nearly all right-handed people and most left-handed people. Broca area, in the inferior frontal lobe, produces speech; damage causes expressive (nonfluent) aphasia, with slow, effortful speech and preserved comprehension. Wernicke area, in the posterior superior temporal lobe, interprets language; damage causes receptive (fluent) aphasia, with fluent but meaningless speech and poor comprehension. Global aphasia affects both. Dysarthria, in contrast, is a motor speech problem with intact language.

The nondominant (usually right) hemisphere handles spatial orientation, attention to the opposite side of space, recognition of faces and emotional tone of speech. Right parietal damage often causes left-sided neglect and anosognosia, in which the patient does not recognize the deficit, raising fall risk.

Exam Tip: Left hemisphere lesions tend to produce aphasia and slow, cautious behavior; right hemisphere lesions tend to produce neglect, impulsivity and poor judgment about safety. Expect fall-prevention items about patients with right hemisphere strokes.

The basal ganglia (caudate, putamen, globus pallidus, with the substantia nigra and subthalamic nucleus) modulate movement; dysfunction causes Parkinson disease, Huntington disease and dystonia. The thalamus relays almost all sensory input to the cortex and helps regulate consciousness; thalamic strokes can cause severe contralateral sensory loss and pain. The hypothalamus controls temperature, hunger, thirst, the pituitary gland and autonomic output, and makes antidiuretic hormone, so hypothalamic or pituitary injury can cause diabetes insipidus. The limbic system, including the hippocampus and amygdala, governs memory and emotion and is a frequent seizure focus.

The brainstem has three parts. The midbrain contains the nuclei of cranial nerves III and IV and pathways for pupil reflexes. The pons contains nuclei of cranial nerves V through VIII and respiratory centers. The medulla contains nuclei of IX through XII and the centers for breathing, heart rate and blood pressure. The reticular activating system runs through the brainstem and maintains wakefulness, so brainstem lesions can cause coma even when the cerebral hemispheres are intact.

The cerebellum coordinates movement, balance and posture on the same side of the body. Cerebellar lesions cause ipsilateral ataxia, dysmetria (overshooting on finger-to-nose), intention tremor, nystagmus and a wide-based gait. Because the posterior fossa is small, cerebellar swelling or bleeding can quickly compress the brainstem and block the fourth ventricle, causing hydrocephalus.

Cranial Nerves and Bedside Tests

The oculomotor nerve deserves special attention. Its parasympathetic fibers run on the outside of the nerve, so compression by an uncal herniation or a posterior communicating artery aneurysm first causes a dilated, sluggish pupil on the same side, followed by ptosis and a "down and out" eye. A sixth nerve palsy is a common false localizing sign of raised ICP because the nerve has a long course along the skull base.

Memory Aid: The classic mnemonic for nerve type is "Some Say Marry Money, But My Brother Says Big Brains Matter More" (Sensory, Sensory, Motor, Motor, Both, Motor, Both, Sensory, Both, Both, Motor, Motor) for nerves I through XII.

Brainstem reflexes are vital in coma assessment and in determining death by neurologic criteria. The corneal reflex tests V (afferent) and VII (efferent). The oculocephalic reflex (doll's eyes) and the oculovestibular reflex (cold calorics) test VIII, III and VI and their brainstem connections. The gag and cough reflexes test IX and X. Never perform the oculocephalic maneuver until cervical spine injury has been excluded.

The spinal cord ends at about L1 to L2 in adults as the conus medullaris; below that, nerve roots form the cauda equina. The cord has gray matter (cell bodies) in an H shape and white matter (tracts) surrounding it.

Major Spinal Cord Tracts

These crossing points explain the incomplete cord syndromes covered in Section 2. A hemisection of the cord causes same-side motor loss and loss of vibration and position sense, with opposite-side loss of pain and temperature (Brown-Sequard syndrome). Damage to the front of the cord spares the dorsal columns, so the patient keeps position sense but loses movement, pain and temperature.

A dermatome is the skin area supplied by one spinal nerve root; a myotome is the muscle group supplied by one root. Useful landmarks include C6 for the thumb, C7 for the middle finger, C8 for the little finger, T4 at the nipple line, T10 at the umbilicus, L4 at the medial leg and knee, L5 at the dorsum of the foot and big toe, and S1 at the lateral foot and heel. Key myotomes include C5 for elbow flexion, C6 for wrist extension, C7 for elbow extension, C8 for finger flexion, T1 for finger abduction, L2 for hip flexion, L3 for knee extension, L4 for ankle dorsiflexion, L5 for great toe extension and S1 for ankle plantar flexion.

Deep Tendon Reflexes and Root Levels

Reflexes are graded 0 (absent), 1+ (diminished), 2+ (normal), 3+ (brisk) and 4+ (very brisk with clonus). A Babinski sign (great toe extension with fanning of the other toes) is abnormal after infancy and indicates an upper motor neuron lesion; it can be normal up to about one to two years of age.

Upper motor neurons run from the cortex to the anterior horn of the spinal cord; lower motor neurons run from the anterior horn to the muscle.

Upper Versus Lower Motor Neuron Lesions

Amyotrophic lateral sclerosis is the classic disease with both upper and lower motor neuron signs. Facial weakness also localizes: an upper motor neuron lesion such as a stroke spares the forehead, while a lower motor neuron lesion of cranial nerve VII, such as Bell palsy, paralyzes the whole side of the face including the forehead.

The sympathetic system ("fight or flight") arises from the thoracolumbar cord, T1 to L2. It raises heart rate and blood pressure, dilates pupils and bronchi, and slows the gut. The parasympathetic system ("rest and digest") arises from cranial nerves III, VII, IX and X and the sacral cord, S2 to S4; it slows the heart, constricts pupils and promotes digestion, bladder emptying and bowel motility. The vagus nerve carries most parasympathetic output to the heart and gut.

Spinal cord injury at T6 or above cuts brain control of the large splanchnic sympathetic outflow, which explains both neurogenic shock (loss of sympathetic tone with unopposed vagal bradycardia) and autonomic dysreflexia (uncontrolled reflex sympathetic surge below the injury). Horner syndrome, from interruption of the sympathetic pathway to the eye, causes ptosis, miosis and loss of sweating on one side; it can signal carotid dissection.

Clinical Scenario: A 58-year-old with a right parietal hemorrhage keeps trying to climb out of bed, denies any weakness and eats only from the right side of the tray. The nurse recognizes left neglect and anosognosia from nondominant parietal damage. Priority actions are fall prevention (bed in low position, frequent rounding, bed alarm per policy), approaching and placing items on the right at first while gradually cueing the patient to scan left, and teaching the family that the patient's denial of deficits is part of the injury, not stubbornness.

The ACA supplies the leg area of the motor strip and the MCA supplies the face and arm area.

Broca damage causes expressive aphasia; Wernicke damage causes fluent receptive aphasia.

The pupil-constricting fibers of cranial nerve III are on the outside of the nerve, so a dilated pupil is an early sign of compression.

Corticospinal and dorsal column tracts cross in the medulla; spinothalamic fibers cross near their level of entry.

Upper motor neuron lesions cause spasticity and hyperreflexia; lower motor neuron lesions cause flaccidity, atrophy and fasciculations.

Injury at T6 or above disrupts sympathetic outflow, setting up neurogenic shock and autonomic dysreflexia.