Chapter 004, Peripheral Nervous System Topics

And then the part behind the mid brain is called the hind brain, hind brain, and it also has a longer name of the rhombencephalon. So the fore brain is going to become the cerebrum. The mid brain is going to become the mid brain.

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Just this part of the brain stem, up top. And then the hind brain will become the rest of the brain. The pons, the medulla, and the cerebellum. So just in case you hear people referring to structures in the brain by these names, that's where those names come from. They're from the developing nervous system.

Here's a drawing of the spinal cord. This kind of long tube that runs down the spine. And there's a number of structures coming out of the spinal cord that I'll talk about next. So those are the parts that make up most of the central nervous system, and everything that's not in the central nervous system we call the peripheral nervous system. And the central nervous system is called that because it's kind of in the center of the body and then the peripheral nervous system is called that because it's going to go out all over the rest of the body.

The peripheral nervous system consists of two types of structures. The first are called nerves. Let me just underline this nerve right here. And these are the long stringy structures that are going to go all over the body. And nerves carry the axons of neurons. The second main structure of the peripheral nervous system are called ganglion.

Ganglion is singular and ganglia is pleural. And ganglia are these lumps that are attached to nerves and they contain the somas of neurons. Now let me just draw that a little differently over on this picture of the spinal cord that have these nerves coming out of it.

So here's one of these lumps, one of these ganglia that contains the somas of some of the neurons in the peripheral nervous system and some of these axons traveling through these nerves are going to be carrying information in to the central nervous system from the periphery. So they're going to bring information in this way from out here in the periphery. And when they do that, we call those afferent neurons, afferent neurons carry information in to the central nervous system. Now other neurons are going to have axons that carry information in the opposite direction.

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So they're going to carry information away from the central nervous system out into the periphery. And neurons whose axons carry information away from the central nervous system we call efferent neurons. Now there are lots of these nerves that are going all over the body.

And you can divide them up in a few different ways. But we usually start by dividing them into the cranial nerves which are nerves that exit the skull or the cranium. So these nerves primarily come out of the brain and they're passing through the skull on their way between the central nervous system and the periphery or the peripheral nerves can be spinal nerves.

And they're coming out of the spinal cord and passing through the spine on their way between the central nervous system and the periphery. And I'll just draw a few of these, but there's actually lots of these. They're paired on both sides of the body. And there are 12 pairs of cranial nerves and 31 pairs of the spinal nerves. Now if we go back to our drawings of the spinal cord here, we can see that the spinal nerves actually form from these two parts which are called spinal nerve roots and there's a root in the front and there's a root in the back.

And in this drawing we're looking from the back. So here's the root in the back that have the ganglia and the way these spinal nerve roots work are that the afferent neurons bringing information into the central nervous system travel through the spinal nerve roots in the back and the efferent neurons that are carrying information away from the central nervous system travel in the spinal nerve roots in the front and then they come together in the spinal nerves, so we call those mixed nerves because they have a mix of afferent and efferent neurons usually.

Now as any of these nerves travel from their proximal origin, proximal just meaning close to the center of the body, toward their distal ends, the word distal just meaning far away from the center of the body, or you can think of the word distant, all the nerves are going to branch repeatedly, so they're going to branch, and then they'll branch, and then they'll branch again, and they'll just keep branching into tinier and tinier branches, because they have a long way to go and have to spread all the way out all the way through the body, and these proximal parts of the nerves are big nerves that we can see with the naked eye.

But once you get to these distal nerves, after they've branched a bunch of times, actually become microscopic, and they're little microscopic nerves that go all over the body connecting the entire body back to the central nervous system. And this is true for almost all of the cranial and the spinal nerves. Oh, I almost forgot here, I have this other drawing to show the cranial nerves.

Here's a drawing of the brain looking up from the bottom, and all of these long stingy looking things coming out of the brain are cranial nerves. They're going to pass through the skull on their way from the brain out into the periphery. I won't draw them all in here, but there are a bunch of these cranial nerves that are going to pass through the skull. Because the vasa nervorum do not reach the center of a nerve, centrally located fascicles are most vulnerable to vascular disorders eg, vasculitis, ischemia.

These disorders result in small-fiber sensory dysfunction sharp pain and burning sensations , motor weakness proportional to atrophy, and less severe reflex abnormalities than in other nerve disorders. The distal two thirds of a limb is affected most. Initially, deficits tend to be asymmetric because the vasculitic or ischemic process is random.

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However, multiple infarcts may later coalesce, causing symmetric deficits multiple mononeuropathy. Toxic-metabolic or genetic disorders usually begin symmetrically. Immune-mediated processes may be symmetric or, early in rapidly evolving processes, asymmetric. Damage to the axon transport system for cellular constituents, especially microtubules and microfilaments, causes significant axon dysfunction. First affected are the smaller fibers because they have greater metabolic requirements at the most distal part of the nerve.

Then, axonal degeneration slowly ascends, producing the characteristic distal-to-proximal pattern of symptoms stocking-glove sensory loss, followed by weakness. However, regrowth may be misdirected, causing aberrant innervation eg, of fibers in the wrong muscle, of a touch receptor at the wrong site, or of a temperature instead of a touch receptor.

Regeneration is impossible when the cell body dies and is unlikely when the axon is completely lost. History should focus on type of symptom, onset, progression, and location, as well as information about potential causes eg, family history, toxic exposures, past medical disorders. Physical and neurologic examination should further define the type of deficit eg, motor deficit, type of sensory deficit, combination. The following are evaluated:. Sensation using pinprick and temperature for small fibers; using vibration and proprioception tests for large fibers. Motor strength noting whether motor weakness is proportional to the degree of atrophy.

Deep tendon reflexes noting type and distribution of reflex abnormalities. Physicians should suspect a peripheral nervous system disorder based on the pattern and type of neurologic deficits, especially if deficits are localized to particular nerve roots, spinal nerves, plexuses, specific peripheral nerves, or a combination. These disorders are also suspected in patients with mixed sensory and motor deficits, with multiple foci, or with a focus that is incompatible with a single anatomic site in the CNS.

Physicians should also suspect peripheral nervous system disorders in patients with generalized or diffuse weakness but no sensory deficits; in these cases, peripheral nervous system disorders may be overlooked because they are not the most likely cause of such symptoms.

Clues that a peripheral nervous system disorder may be the cause of generalized weakness include the following:. Patterns of generalized weakness that suggest a specific cause eg, predominant ptosis and diplopia, which suggest early myasthenia gravis. Symptoms and signs other than weakness that suggest a specific disorder or group of disorders eg, cholinergic effects, which suggest organophosphate poisoning.

Deficits in a stocking-glove distribution, which suggest diffuse axonal disorders or polyneuropathy. These deficits suggest an upper motor neuron disorder as the cause of weakness. Hyporeflexia is consistent with peripheral nervous system deficits but is nonspecific. Diffuse disorders eg, toxic-metabolic, hereditary, infectious, or inflammatory disorders; most immune-mediated disorders. Focal disorders eg, mononeuropathies , plexopathies.

Diffuse peripheral polyneuropathies , possibly axonal.

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Disproportionate weakness of proximal muscles eg, difficulty climbing stairs or combing hair with no sensory deficits. Possibly disorders of the neuromuscular junction if eye movements are affected. Weakness proportional to atrophy; disproportionately mild reflex abnormalities, usually more distal than proximal. Vascular disorders eg, vasculitis , ischemia, hypercoagulable states.

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Usually, nerve conduction studies and electromyography collectively called electrodiagnostic testing are done. These tests help identify level of involvement nerve, plexus, root and distinguish demyelinating disorders very slow conduction from axonal disorders. Other testing, such as imaging, depends on whether a CNS lesion must be ruled out eg, MRI if all limbs are affected, to rule out cervical spinal cord compression. Nerve biopsy is occasionally done to help differentiate demyelinating from vasculitic large-fiber neuropathies. If vasculitis is a consideration, the biopsy specimen should include skin and muscle to increase the likelihood of a definitive diagnosis.

If a small-fiber neuropathy is suspected, skin punch biopsy can be done; loss of nerve endings supports that diagnosis. If clinical findings and electrodiagnostic test results are inconclusive, do a biopsy nerve biopsy for suspected large-fiber neuropathy or skin punch biopsy for suspected small-fiber neuropathy. Patients with weakness but no sensory deficits can be evaluated with electrodiagnostic testing.

Electrodiagnostic testing helps differentiate peripheral nervous system disorders from other causes of weakness and helps differentiate among peripheral nervous system disorders eg, root, plexus, peripheral nerve, neuromuscular junction, muscle fiber. It also helps differentiate between axonal and demyelinating peripheral neuropathies.

Treatment is directed at the underlying disorder when possible.

Otherwise, treatment is supportive. A multidisciplinary team approach helps patients cope with progressive neurologic disability:. Occupational therapists can recommend adaptive braces and walking devices to help with activities of daily living. If respiratory weakness develops, forced vital capacity is measured, and pulmonary or intensive care specialists help assess whether intensive care, noninvasive respiratory support eg, bilevel positive airway pressure , and tracheostomy with full ventilatory support are needed.

Early in fatal disorders, health care practitioners must talk frankly with patients, family members, and caregivers to determine the level of intervention acceptable. Patients are encouraged to put their decisions in writing advance directives before they become incapacitated. These decisions should be reviewed and confirmed at various stages of the disorder. Peripheral nervous system disorders are often suspected based on clinical findings eg, stocking-glove distribution, hyporeflexia, distal muscle weakness and wasting, localization to a peripheral nerve distribution.

If patients have profound motor weakness with minimal atrophy and areflexia, consider acquired demyelinating polyneuropathy. If patients have abnormal pain and temperature sensation and atrophy in proportion to weakness sometimes with disproportionate preservation of reflexes , consider a vasculitic or ischemic neuropathy. If patients have chronic progressive muscle weakness, fasciculations, muscle atrophy, and no sensory deficits, consider motor neuron disease.

Nerve conduction studies and electromyography help identify level of involvement root, plexus, peripheral nerve, neuromuscular junction, muscle fiber and help distinguish demyelinating from axonal disorders. The most common types of muscle cramps are benign idiopathic leg cramps and which of the following? Tap to switch to the Consumer Version. Overview of Peripheral Nervous System Disorders. This is the Professional Version. Click here for the Consumer Version. A motor unit consists of.

An anterior horn cell. Peripheral nerve disorders can result from damage to or dysfunction of the one of the following: Central core disease, centronuclear myopathy, nemaline myopathy very rare. Deficits defined by history and examination. Attention to clinical clues to peripheral nervous system disorders. The following are evaluated: