How to Localize Neurologic Lesions by Physical Examination

Article Author:
Muhammad Zaman Khan Assir
Article Editor:
Joe M Das
Updated:
5/29/2019 11:07:45 PM
PubMed Link:
How to Localize Neurologic Lesions by Physical Examination

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 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 is of paramount importance in the localization of a neurological lesion. Medical students are often perplexed with the complexity of this knowledge. This video lecture on the localization of a neurological lesion is aimed at delivering a succinct and easy to understand overview of the subject.[1][2][3][4]

Function

The nervous system is divided into the central nervous system (CNS) and peripheral nervous system. The central nervous system comprises of the brain and spinal cord. Cranial and spinal nerves make up the peripheral nervous system.

The brain consists of 2 cerebral hemispheres, brain stem, and cerebellum. The cerebral cortex is a convoluted structure that has multiple tortuous folds called gyri separated by deep grooves called sulci. Central sulcus separates frontal lobe from the parietal lobe, and the Sylvian fissure marks the upper boundary of the temporal lobe. An arbitrary line separates occipital lobe from parietal and temporal lobes. 

Precentral gyrus serves as primary motor cortex and is the command and control center for voluntary movements. Pyramidal cells in the layer V of 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 parietal and temporal lobes analyzes sensory input related to speech and is called Wernicke's area. Brain stem consists of the midbrain, pons, and medulla. Some cranial nerves leave brain stem.

Descending fibers of 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 right cerebral cortex innervate left spinal motor nuclei and vice versa. Spinal motor nuclei innervating skeletal muscles of upper and lower limbs receive upper motor neuron innervation from the contralateral side only. 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 one side, cranial motor nuclei will continue to receive upper motor supply from the other side. The nucleus of the facial nerve, however, can be considered a hybrid. The upper half of facial nucleus, like other cranial motor nuclei, 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. 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 upper and lower limbs, respectively.

Sensory pathways consist of the lateral spinothalamic tract and dorsal column-medial lemniscal pathway. Pain and temperature sensations are carried through the lateral spinothalamic tract, while 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 make 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, 3. 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 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, upper motor neuron type of weakness is characterized by normal muscle bulk, hypertonia, hyperreflexia, clonus and an extensor plantar response (positive Babinski’s sign). Furthermore, 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. Uppermost dermatomal level of accompanying sensory loss can further localize 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 that can be partial or complete. Compressive myelopathy can result from compression from outside like a vertebral fracture, vertebral metastasis or subdural abscess or hematoma, or from inside like 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 will result in left facial weakness of lower motor neuron type and right-sided hemiplegia. Similarly, a lesion in left midbrain will result in left-sided oculomotor weakness with right hemiparesis and right facial weakness of upper motor neuron type. This constellation of signs is called Weber syndrome. Lesions above the level of brainstem result in uncrossed hemiplegia. For example, lesion in the left internal capsule would result in right hemiplegia and right facial weakness of upper motor neuron type. A left cortical lesion may also result in cortical dysfunction in addition to right hemiparesis and facial weakness of 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.



References

[1] Fasano A,Laganiere SE,Lam S,Fox MD, Lesions causing freezing of gait localize to a cerebellar functional network. Annals of neurology. 2017 Jan;     [PubMed PMID: 28009063]
[2] Kawasaki AK, Diagnostic approach to pupillary abnormalities. Continuum (Minneapolis, Minn.). 2014 Aug;     [PubMed PMID: 25099106]
[3] Newman N,Biousse V, Diagnostic approach to vision loss. Continuum (Minneapolis, Minn.). 2014 Aug;     [PubMed PMID: 25099095]
[4] Kumar A,Chandra PS,Sharma BS,Garg A,Rath GK,Bithal PK,Tripathi M, The role of neuronavigation-guided functional MRI and diffusion tensor tractography along with cortical stimulation in patients with eloquent cortex lesions. British journal of neurosurgery. 2014 Apr;     [PubMed PMID: 24024910]
[5] Weiss N,Galanaud D,Carpentier A,Tezenas de Montcel S,Naccache L,Coriat P,Puybasset L, A combined clinical and MRI approach for outcome assessment of traumatic head injured comatose patients. Journal of neurology. 2008 Feb;     [PubMed PMID: 18283406]
[6] Balakrishnan G,Kadadi BK, Clinical examination versus routine and paraspinal electromyographic studies in predicting the site of lesion in brachial plexus injury. The Journal of hand surgery. 2004 Jan;     [PubMed PMID: 14751117]
[7] Assmus H, [Neurological examination methods of the hand]. Kongressband. Deutsche Gesellschaft fur Chirurgie. Kongress. 2002;     [PubMed PMID: 12704904]