Continuing Education Activity

The human brain has a highly complex structure. It contains billions of neurons wired together through trillions of connections. Each portion of the brain has a distinct set of functions. Damage to a part of the brain results in characteristic clinical manifestations. Knowledge of neuroanatomy, functions of different parts of the brain, and clinical manifestations resulting from damage to a part of the brain are paramount in localizing a neurological lesion. Health professionals are often challenged with the complexity of this knowledge. This activity highlights the role of the physical examination in the localization of a neurological lesion and aims to deliver a succinct and easy-to-review overview of the subject.

Objectives:

• Identify the functions of the different parts of the brain.

• Assess the technique of performing a thorough neurological exam.

• Evaluate the clinical significance of a neurological exam.

• Communicate interprofessional team strategies for improving care coordination among health professionals with challenging neurologic conditions.

Introduction

The human brain has a highly complex structure. It contains billions of neurons wired together through trillions of connections. Each portion of the brain has a distinct set of functions. Damage to a part of the brain results in characteristic clinical manifestations. Knowledge of neuroanatomy, functions of different parts of the brain, and set of clinical manifestations resulting from damage to a part of the brain are of paramount importance in the localization of a neurological lesion. Medical students are often perplexed by the complexity of this knowledge. This accompanying video lecture on the localization of a neurological lesion aims to deliver a succinct and easy-to-understand overview of the subject (see Video. Localization of Lesions Lecture).[1][2][3][4]

Function

The nervous system is divided into the central nervous system (CNS) and the peripheral nervous system. The CNS is comprised of the brain and spinal cord. Cranial and spinal nerves make up the peripheral nervous system. The brain consists of 2 cerebral hemispheres: the brain stem and the cerebellum. The cerebral cortex is a convoluted structure with multiple tortuous folds called gyri separated by deep grooves called sulci. The central sulcus separates the frontal lobe from the parietal lobe, and the Sylvian fissure marks the upper boundary of the temporal lobe. An arbitrary line separates the occipital lobe from the parietal and temporal lobes. 

The precentral gyrus serves as the primary motor cortex and is the command and control center for voluntary movements. Pyramidal cells in layer V of the cerebral cortex innervate lower motor neurons located in the cranial and spinal motor nuclei through corticobulbar and corticospinal tracts, respectively. These pyramidal cells are called upper motor neurons. The distribution of these pyramidal cells follows a unique topographic pattern. Upper motor neurons that control lower motor neurons of the lower limb are located on the medial side, and those innervating lower motor neurons of the upper limb are located laterally. An area on the lateral surface of the dominant frontal lobe, the left frontal lobe in most individuals, is the motor control center for speech. It is called Broca’s area. Another area at the junction of the parietal and temporal lobes analyzes sensory input related to speech and is called Wernicke's area. The brain stem consists of the midbrain, pons, and medulla. Some cranial nerves leave the brain stem.

Descending fibers of the corticospinal tract travel from the cerebral cortex to corona radiata, posterior limb of the internal capsule, cerebral peduncles, pons, and medulla. At the lower part of the medulla, most of these fibers cross the midline, continue as the lateral corticospinal tract, and descend through the white matter of the cord to innervate the anterior horn cells. This crossing over of corticospinal tract fibers is called pyramidal decussation. Resultantly, pyramidal cells of the right cerebral cortex innervate left spinal motor nuclei and vice versa. Spinal motor nuclei innervating skeletal muscles of the upper and lower limbs receive upper motor neuron innervation only from the contralateral side. Lower motor neurons of cranial nerves, on the other hand, are innervated by corticobulbar fibers from both sides. Therefore, despite damage to corticobulbar fibers on 1 side, cranial motor nuclei continue to receive upper motor supply from the other side. The nucleus of the facial nerve, however, can be considered a hybrid. Like other cranial motor nuclei, the upper half of the facial nucleus receives bilateral upper motor neuron innervation. On the other hand, the lower half receives innervation only from the contralateral side. 

Medulla oblongata passes through the foramen magnum and continues as the spinal cord. The spinal cord has multiple segments. Each segment gives away a pair of spinal nerves. There are 8 cervical, 12 thoracic, 5 lumbar, 5 sacral, and 2 coccygeal segments. Looking at the cross-section, the spinal cord has a central gray matter that contains cell bodies of spinal nuclei and peripheral white matter that contains myelinated axons. The anterior horn of the gray matter contains spinal motor nuclei; axons of these neurons innervate skeletal muscles and are called lower motor neurons. Axons of these neurons travel through the anterior root of the spinal nerves and form brachial and lumbosacral plexuses that innervate the upper and lower limbs, respectively.

Sensory pathways include the lateral spinothalamic tract and the dorsal column medial lemniscal pathway. Pain and temperature sensations are carried through the lateral spinothalamic tract, while the dorsal column tract carries fine touch, vibration, and proprioception. First-order neurons are located in the dorsal root ganglion of spinal nerves. Second-order neurons for spinothalamic and dorsal column tracts are located in the posterior horn of the gray matter of the spinal cord and nucleus gracilis and cuneatus in the medulla, respectively. Exons of second-order neurons cross the midline and synapse with third-order neurons in the thalamus on the contralateral side.

Issues of Concern

Three questions are needed to be addressed sequentially to localize a neurological lesion. First, what is the lesion? This includes defining the pattern and distribution of weakness, type of weakness (upper motor neuron versus lower motor neuron type), and presence or absence of sensory deficit. Second, where is the lesion? This question addresses the anatomical localization of a neurological lesion. Third, why has the lesion occurred? This encompasses the etiological basis of a neurological lesion.

Clinical Significance

Examination of the motor system of a limb includes checking for muscle bulk and fasciculation, muscle tone at joints, the power of muscle groups, deep tendon reflexes, clonus, plantar response, and coordination. In cases of a lower motor neuron type weakness, there is early muscle wasting, fasciculations, hypotonia, hyporeflexia, and a normal plantar response. On the other hand, the upper motor neuron type of weakness is characterized by normal muscle bulk, hypertonia, hyperreflexia, clonus, and an extensor plantar response (positive Babinski sign). Furthermore, the preservation of deep tendon reflexes distinguishes myopathy from neuropathy. Lower motor neuron type weakness can result from any pathology of anterior horn cells, spinal nerve roots, plexus, or peripheral nerves. An upper motor neuron paraplegia can result from myelopathy involving the thoracic spinal cord, while cervical myelopathy would result in quadriplegia. The uppermost dermatomal level of accompanying sensory loss can further localize the lesion to the corresponding spinal segment. Myelopathy is further classified into compressive and non-compressive myelopathy. An example of non-compressive myelopathy is transverse myelitis, which can be partial or complete. Compressive myelopathy can result from compression from the outside, like a vertebral fracture, vertebral metastasis subdural abscess, or hematoma, or from the inside with conditions such as syringomyelia or hematomyelia.

Hemiplegia can result from a unilateral lesion of the brain stem, internal capsule, or cerebral cortex. Brain stem lesions result in crossed hemiplegia. For example, a left pontine lesion results in left facial weakness of lower motor neuron type and right-sided hemiplegia. Similarly, a lesion in the left midbrain results in left-sided oculomotor weakness with right hemiparesis and right facial weakness of the upper motor neuron type. This constellation of signs is called Weber syndrome. Lesions above the level of the brainstem result in uncrossed hemiplegia. For example, a lesion in the left internal capsule would result in right hemiplegia and right facial weakness of the upper motor neuron type. A left cortical lesion may also result in cortical dysfunction in addition to right hemiparesis and facial weakness of the upper motor neuron type.[5][6][7]

Enhancing Healthcare Team Outcomes

Clinicians, including nurses, must know how to perform a neurological exam. The exam can point to the location of the problem. However, it is important to confirm the pathology with some type of imaging study. The physical exam alone should not be relied upon for treatment.