Neurology
Contents: Introduction Somatosensory
Introduction Neurology The study of the structure, function, and pathology of the nervous system and skeletal muscle and the treatment of their disorders. Also, NEUROLOGIA.
History and development The modern science of neurology has developed in the past two centuries. The first scientific studies of nerve function in animals were done in the early 18th century by Stephen Hales and Robert Whytt. But clinical neurology was still relatively unexplored territory until the middle of the 19th century.
Important contributions to neurological knowledge were made in the mid- and late 19th century. New knowledge was gained about the causes of aphasia, epilepsy, and about motor problems arising from brain damage. The mapping of the functional areas of the brain through selective electrical stimulation also began at this time.
Despite these contributions, however, most new knowledge of the brain and nervous functions came from studies of animals and from the microscopic analysis of nerve cells.
The diagnosis of neurological disease was greatly improved by Hans Berger's invention of the electroencephalograph, which records electrical brain activity.
With this device, with the analysis of cerebrospinal fluid obtained by the spinal tap, and with the development of cerebral angiography (to see the blood vessles in the brain), neurologists were able to increase the precision of their diagnoses and develop specific therapies and rehabilitative measures.
Further aiding the diagnosis of brain disorders were the development of computerized axial tomography (CAT scans) in the early 1970s and nuclear magnetic resonance (NMR) imaging in the 1980s, both of which yielded detailed, noninvasive views of the inside of the brain.
Another major development was the introduction of specific drug therapies for neurological conditions. The identification of chemical agents in the central nervous system and the elucidation of the roles these substances play in the transmitting and blocking of nerve impulses led in the mid- and late 20th century to a wide array of drugs that could correct or alleviate various neurological disorders.
Neurological surgery, or neurosurgery, is a medical specialty related to neurology. It is perhaps the most difficult and delicate of the surgical disciplines, but it too has benefited from CAT scans and other increasingly precise methods of locating lesions and other abnormalities in nervous tissues.
However, the past several years have witnessed a dramatic explosion of new knowledge in biochemical, physiological, pharmacological, and molecular approaches to the nervous system.
These basic science advances have been translated into new ways of diagnosing human neurological disease, new methods for treating previously untreatable diseases, and new insights into the effective control of stroke, dementia, epilepsy, parkinsonism, and neuromuscular diseases.
But neurological disorders have always been among the most subtle and baffling of human illnesses, and despite continuing advances in their field, neurologists remained unable to effectively treat many disorders of the nervous system.
The future form of neurology will be shaped by knowledge of the human genome and proteome.
Localization of the Lesion of Somatosensory
Definition
Somatosensory includes sensations of touch or pressure, vibration, joint position, pain, temperature, and more complex functions that rely on these primary sensory modalities (twopoint discrimination, stereognosis, graphesthesia); it excludes special senses such as smell, vision, taste, and hearing.
A. Peripheral receptors
There are three different categories of the somatosensory system. The first, discriminative touch, is the perception of pressure, vibration, and texture.
This system relies on four different receptors in the skin. They are: Meissner's corpuscles Pacinian corpuscles Merkel's disks Ruffini endings
The first two are considered rapidly adapting (they quickly stop firing in response to a constant stimulus) and the second two are considered slowly adapting (they do not stop firing).
To put this into an example, if you lay your pen down in your palm, the Meissner's and Pacinian corpuscles will fire rapidly as it first touches down, to let you know something has landed.
If the pen lays still, they will stop firing almost right away. The Merkel's and Ruffini endings, however, will continue to fire to let you know that something is still there.
The pain and temperature system does not have specialized receptor organs. Instead, it uses free nerve endings throughout skin, muscle, bone, and connective tissue to perceive changes in temperature and pain peptides.
Although pain will result from damage to a free nerve ending, in reality most pain is a result of substances released by damaged tissues: histamine, and substance P. The free nerve ending has receptors for these substances and lets you know when tissue has been damaged.
The third modality, proprioceptive sensation, relies on receptors in muscles and joints. The muscle spindle is the major stretch receptor within muscles, and just like the cutaneous receptors, it has a rapidly-adapting and slowly-adapting component.
There are also Golgi tendon organs and joint afferents to monitor stresses and forces at the tendons and joints.
B.
Axon diameters
Sensory axons can be classified according to diameter and therefore conduction velocity.
The largest and fastest axons are called Aα , and include some of the proprioceptive neurons, such as the stretch receptor. The second largest group is called Aβ , which includes all of the discriminative touch receptors.
Pain and temperature include the third and fourth groups, Aδ and C fibers. There are two subtypes of pain. "Fast pain", carried by the Aδ fibers, is the instantaneous pain that makes your arm jerk back before you even realized you were burned. It is sharp and piercing and over quickly.
"Slow pain" is carried by C fibers. C fibers are not only small, they are unmyelinated (the only sensory axons without myelin), so their conduction velocity is quite slow.
Slow pain is primarily mediated by those tissue-damage peptides listed above, and can go on indefinitely. It is distressing, it can be dull and aching, and it does not trigger withdrawal reflexes like the fast pain.
As the dorsal root enters the cord (all sensory information comes in via the dorsal root, and all sensory cell bodies are in the dorsal root ganglion), the fibers sort themselves out by diameter.
The largest fibers enter the cord most medially, and the smallest fibers enter most laterally. From there, the three modalities take very different paths, so we must look at each one separately.
C.The discriminative touch system
Discriminative touch includes touch, pressure, and vibration perception, and enables us to "read" raised letters with our fingertips, or describe the shape and texture of an object without seeing it.
Discriminative touch system is carried in the spinal cord includes the entire body from the neck down; face information is carried by cranial nerves, and we will come back to it later.
Sensation enters the periphery via sensory axons. All sensory neurons have their cell bodies sitting outside the spinal cord in a clump called a dorsal root ganglion. There is one such ganglion for every spinal nerve. The sensory neurons are unique because unlike most neurons, the signal does not pass through the cell body. Instead the cell body sits off to one side, without dendrites, and the signal passes directly from the distal axon process to the proximal process.
The proximal end of the axon enters the dorsal half of the spinal cord, and immediately turns up the cord towards the brain. These axons are called the primary afferents , because they are the same axons that brought the signal into the cord. (In general, afferent means towards the brain, and efferent means away from it.) The axons ascend in the dorsal white matter of the spinal cord.
At the medulla, the primary afferents finally synapse. The neurons receiving the synapse are now called the secondary afferents . The secondary afferents cross immediately, and form a new tract on the other side of the brainstem.
This tract of secondary afferents will ascend all the way to the thalamus, which is the clearinghouse for eveything that wants to get into cortex. Once in thalamus, they will synapse, and a third and final neuron will go to cerebral cortex, the final target.
The key points are that the primary afferents ascend all the way to the medulla, on the is pilateral side of the cord, in the posterior columns.
The secondary afferents cross in the medulla and ascend as the medial lemniscus. In the thalamus they synapse in the VPL (the ventroposterior lateral nucleus) and finally ascend to cortex.
D. The pain and temperature system:
This system shares one major rule with the discriminative touch system: primary afferents synapse ipsilaterally, then secondary afferents cross. SYNAPSE, then CROSS. The crossings just occur at different levels.
Pain afferents (all of the following applies to temperature as well) enter the cord laterally, due to their small size, and synapse more or less immediately. "More or less", because they actually can travel one or two segments up or down the cord before synapsing.
Lissauer's tract is the tract carrying these migrating axons, but they are only in the tract for a short time. Within one or two levels, they enter the dorsal horn and synapse.
These are the secondary afferents (purple, below) which will carry the signal to the thalamus. The secondary afferents from both layers cross to the opposite side of the spinal cord and ascend in a tract called the spinothalamic tract. Tracts are always labeled from beginning to end.
The spinothalamic system enters the VPL, synapses, and is finally carried to cortex by the thalamocortical neurons. Here is a schematic of the entire pathway:
E.
The proprioceptive system:
The proprioceptive system arises from primarily the A afferents entering the spinal cord. These are the afferents from muscle spindles, Golgi tendon organs, and joint receptors.
The axons travel for a little while with the discriminative touch system, in the posterior columns. Within a few segments, however, the proprioceptive information slips out of the dorsal white matter and synapses. After synapsing it ascends without crossing to the cerebellum.
Exactly where the axons synapse depends upon whether they originated in the legs or the arms. Leg fibers enter the cord at sacral or lumbar levels, ascend to the upper lumbar segments, and synapse in a medial nucleus called Clarke's nucleus
The secondary afferents then enter the dorsal spinocerebellar tract on the lateral edge of the cord.
Fibers from the arm enter at cervical levels and ascend to the caudal medulla. Once there they synapse in a nucleus called the external cuneate nucleus, and the secondary axons join the leg information in the dorsal spinocerebellar tract.
The spinocerebellar tract stays on the lateral margin of the brainstem all the way up the medulla. Just before reaching the pons, it is joined by a large projection from the inferior olive.
These axons together make up the bulk of the inferior cerebellar peduncle, which grows right out of the lateral medulla and enters the cerebellum.
F. SENSORY CHANGES & THEIR SlGNIFICANCE
It is Important to determine the nature and distribution of any sensory change. Failure to find clinical evidence of sensory loss in patients with sensory symptoms must never be taken to imply that the symptoms have a psychogenic basis. Sensory symptoms often develop well before the onset of sensory signs.
(1).Peripheral Nerve Lesions
A. Mononeuropathy:
In patients with a lesion
of a single peripheral nerve, sensory loss is usually less than would have been predicted on anatomic grounds because of overlap from adjacent nerves.
B. Polyneuropathy: In patients with polyneuropathies, sensory loss is generally symmetric and is greater distally than proximally-as suggested by the term stocking-and-glove sensory loss.
As a general rule the loss will have progressed almost to the knees before the hands are affected.
Certain metabolic disorders preferentially involve small nerve fibers that subserve pain and temperatme appreciation. Sensory loss may be accompanied by a motor deficit and reflex changes.
(2).
Root Involvement
Nerve root involvement produces impairment of cutaneous sensation in a segmental pattern, but because of overlap there is generally no loss of sensation unless two or more adjacent roots are affected.
Pain is often a conspicuous feature in patients with compressive root lesions. Depending on the level affected, there may be loss of tendon reflexes , and if the anterior roots are also involved, there may be weakness and muscle atrophy .
(3). Cord Lesion
In patients with a cord lesion, there may be a transverse sensory level. The level of a sensory deficit affecting the trunk is best determined by careful sensory testing over the back rather than the chest and abdomen.
A. Central Cord Lesion: With a central cord lesion--such as occurs in tumors there is characteristically a loss of pain and temperature appreciation with sparing of other modalities.
This loss is due to the interruption of fibers conveying pain and temperature that cross from one side of the cord to the spinothalamic tract on the other.
Such a loss is usually bilateral. may be asymmetric, and involves only the fibers of the involved segments. It may be accompanied by lower motor neuron weakness in the muscles supplied by the affected segments and sometimes by a pyramidal and posterior column deficit below the lesion .
B. Anterolateral Cord Lesion: Lesions involving the anterolateral portion of the spinal cord (lateral spinothalamic tract) can cause contralateral impairment of pain and temperature appreciation in segments below the level of the lesion.
C. Anterior Cord Lesion: With destructive lesions involving predominantly the anterior portion of the spinal cord, pain and temperature appreciation are impaired below the level of the lesion from lateral spinothalamic tract involvement.
In addition, weakness or paralysis of muscles supplied by the involved segments of the cord results from damage to motor neurons in the anterior horn.
D. Posterior Column Lesion: A patient with a posterior column lesion may complain of a tight or bandlike sensation in the regions corresponding to the level of spinal involvement and sometimes also of paresthesias (like electric shocks) radiating down the extremities on neck flexion (Lhermitte's sign).
There is loss of vibration and joint position sense below the level of the lesion, with preservation of other sensory modalities. The deficit may resemble that resulting from involvement of large fibers in the posterior roots.
E.
Cord Hemisection: Lateral hemisection of he cord leads to BrownSéquard's sydrome.
Below the lesion there is ipsilateral pyramidal deficit and disturbed appreciation of vibration and joint position sense. with contralateral loss of pain and temperature appreciation that begins two or three segments below the lesion .
(4). Brainstem Lesion
Sensory disturbances may be accompanied by a motor deficit, cerebellar signs. and cranial nerve palsies when the lesion is in the brainstem. In patients with lesions involving the spinothalamic tract in the dorsolateral medulla and pons, pain and temperature appreciation are lost in the limbs and trunk on the opposite side of the body.
When such a lesion is located in the medulla, the spinal trigeminal nucleus, on the same side of the face as the lesion. The result is a crossed sensory deficit that affects the ipsilateral face and contralateral limbs.
In contrast, spinothalamic lesions above the spinal trigeminal nucleus affect the face,limbs, and trunk contralateral to the lesion. With lesions affecting the medial lemniscus, there is loss of touch and proprioception on the opposite side of the body.
In the upper brainstem, the spinothalamic tract and medial lemniscus run together so that a single lesion may cause loss of all superficial and deep sensation over the contralateral side of the body .
(5). Thalamic Lesions
Thalamic lesions may lead to loss or impairment of all forms of sensation on the contralateral side of the body. Spontaneous pain, sometimes with a particularly unpleasant quality may occur on the affected side.Patients may describe it as burning, tearing.knifelike, or stabbing, but often have difficulty characterizing it.
(6). Lesions of the Sensory cortex
Disease limited to the sensory cortex impairs discriminative sensory function on the opposite side of the body. Thus, patients may be unable to localize stimuli on the affected side or to recognize the position of different parts of the body.
They may not be able to recognize objects by touch or to estimate their size, weight, consistency, or texture. Cortical sensory disturbances are usually more conspicuous in the hands than in the trunk or proximal portions of the limbs.
Finally, it should be noted that sensory disturbances are often suggested to the patient by the examiner's own expectations. Such findings can be particularly misleading because they may be neuroanatomically correct. One helpful approach is to have the patient outline on the body the extent of any perceived sensory disturbance before formal sensory testing is undertaken.