PNS Ws Flashcards
WHta is a schwann cell?
Myelinating cell of PNS + support cells of peripheral neurons.. Can be myelinating or non-myelinating. Functional analogues of oligodendrocytes in the CNS.
WHta is. LMN?
Motor neurons that directly innervate muscle eg, a motor neurons of ventral horn.
WHat is a somatic motor unit
motor unit defined as an a motor neuron and all of the myofibres that it innervates. Frequently, different motor units, of different subtypes, function together to coordinate contraction of given muscle. All the a motor neurons and fibres it innervates is motor unit.
What is a dorsla root ganglion
Spinal ganglion. Collection of neuronal cell bodies of pseudouniplolar primary somatosensory neurons in turnk.
What is a myelin basic protein
believed to be important in process of myelination of nerve sin NS. Protein that sticks together membrane that’s wrapped dupon one another.
What is a perineuriam
Layer of CT within a nerve that surrounds a nerve fascicle. Within it lies the endoneurum, composed of endoneural bundles of CT(mostly collagen) and endoneural fluid of pns (CSF).
WHat is a growth cone
Specialised motile tip of an axon of a growing or regenerating neuron.
Henry head area
Head areas- areas of skin exhibiting reflex hyperesthesia and hyperalgesia due to visceral disease. Head lines- bands of cutaneous hyperesthesia associated with acte or chronic inflammation of viscera.
Do the nerve sin CNS/PNS regenerate
CNS axons do not spontaneously regenerate after injury in adult mammals. PNS axons readily regenerate, allowing recovery of function after PNS nerve damage.
Peirherla nerve labelled
Whats happening in these axons
Degeneration becomes visible via blebbing about 40hours after injury. Degeneration occurs proximally and distally.
Regrowth almost perfect with same patterns synapse/ growth
What can you conclude about the organisation of motor endplates after nerve lesion?
Mycobacterium leprae. Hansen disease- leprosy. Macrophages are filled with acid fast bacilli (“globi”)
A poorly formed granuloma is seen around a peripheral nerve within the dermis. The bacilli (Mycobacterium leprae) grow best just below body temperature, preferring the cooler skin and peripheral nerves. Hypopigmented patches or macular lesions with decreased sensation develop on the face, extremities, and trunk. Nodular disfiguring lesions occur with one form in which many macrophages are filled with numerous acid-fast bacilli (“globi”) (◄). In the tuberculoid form with more robust immune response, the acid-fast organisms are sparse. Seen here is the “borderline” form, with some organisms and some epithelioid cells. It is possible to control with drug therapy.
Peripheral nerve with axonal sprouting. Clusters of regrowing axons.
Here is a cross-section of a peripheral nerve following transection (axonotmesis), with clusters of regrowing axons (▼) surrounded by the basement membrane of a Schwann cell. Such small clusters of thinly myelinated fibers represent axonal sprouting. With ongoing disease from neuropathies, degeneration and regeneration may coexist.
Varicella zoster virus infection – shingles. Reactivation virus produces hemorrhagic lesions of dorsal root ganglia
This viral infection is typically self-limited, but the virus persists and becomes latent in dorsal root ganglia. It can be severe in immunocompromised individuals, infants, and adults. A postherpetic neuralgia syndrome persists in approximately 10% of infected individuals. In some patients, activation of the virus later in life, particularly with immune compromise, can produce a painful condition seen as a vesicular eruption in a dermatome distribution innervated by an infected ganglion. Reactivated virus produces hemorrhagic lesions (♦) of these ganglia, as shown here. In some immunocompromised patients, acute encephalitis can occur.
Malignant peripheral nerve sheath tumour. Soft tissue sarcoma arising in adults. A fusiform mass in relation to nerve.
This is a soft-tissue sarcoma arising in adults over a wide age range, with male predominance, and most often in extremities, as a fusiform mass in relation to a nerve. Some cases arise in neurofibromatosis type 2. Microscopically it is composed of plump spindles cells in a fascicular pattern. There may be areas of necrosis. Immunohistochemical staining for S100 and NSE is usually positive. When the proliferation marker MIB-1 is found in greater than 5% of cells, it is considered high grade.
guillain-barre neuropathy
Neuritis secondary to an acute inflammatory demyelinating polyneuropathy is shown in a longitudinal section of peripheral nerve with lymphocytic infiltrates (▲) that damage the nerve, followed by macrophages that strip off the myelin lamellae, leading to demyelination with relative preservation of axons in most cases. There is an acute ascending paralysis that occurs over days, advancing distally to proximally. Respiratory paralysis is life threatening. A bacterial (Campylobacter jejuni) or viral (cytomegalovirus) illness may precede the onset of this disease. Recovery occurs in most patients receiving ventilatory support.
Diabetic neuropathy. Diffuse loss of darkly staining thickyly and thinly myelinated fibres. Leads to typical for the progressive distal sensorimotor polyneuropathy. Microvascular disease -> thickened walls of small blood vessels
This plastic embedded cross-section of nerve shows diffuse loss of darkly staining thickly and thinly myelinated fibers (►) typical for the progressive distal sensorimotor polyneuropathy that accompanies this condition. Note the microvascular disease with thickened walls of small vessels (◄). End glycosylation of proteins and sorbitol accumulation in cells not requiring insulin for glucose uptake can underlie the pathogenesis of this neuropathy, driven by persistent hyperglycemia.
Denervation atrophy. “Grouped atrophy” . Decrease of muscle fibres that have lost their innervation from a LMN. Could result from traumatic nerve injury, peripheral neuropathy, or lower motor neurone disease.
This modified Gomori trichrome stain shows the neurogenic form of skeletal muscle atrophy, with the characteristic pattern of “grouped atrophy” (▼) of muscle fibers that have lost their innervation from a lower motor neuron. These affected muscle fibers do not die, but “downsize” with loss of actin and myosin, becoming small and angular. Could result from traumatic nerve injury, peripheral neuropathy, or a lower motor neuron disease, such as amyotrophic lateral sclerosis. Remaining axons may reinnervate myofibers as a single fiber type (“type grouping”).
Chronic inflammatory demyelinating polyneuropathy.
In this sural nerve biopsy on cross section, note the “onion bulb ” formation from excessive proliferation of Schwann cells following recurrent demyelination and remyelination from macrophage response to immunoglobulin (IVIg) deposition. This is the most common chronic acquired inflammatory peripheral neuropathy, lasting from months to years, usually with relapses and remissions. There is a symmetric, mixed sensorimotor polyneuropathy. An underlying autoimmune disorder may be present. Peak incidence is 40 to 60 years of age. Therapies include corticosteroids, plasma exchange, and intravenous immunoglobulin (IVIg).
Amyloid neuropathy . Thickening of endoneurial vessels from deposition of amorphous material within vascular walls. Axonal degeneration occurs over time. The causative agent can be due to breakdown or lack proteins.
Note the thickening of endoneurial vessels from deposition of amorphous material within the vascular walls (▲). This can involve the endoneurial vessels of a peripheral nerve. Axonal degeneration occurs over time. The causative agent can be derived from the breakdown of various proteins, such as light chains with multiple myeloma, or serum proteins when there is a chronic inflammatory condition, such as tuberculosis or rheumatoid arthritis.
Wallerian degeneration. In this distal nevre segment, small aonal and myelin fragments lie within myelin ovoids as vacuolar digestion chambers. Regeneration proceeds along the course of degenerating axon.
This occurs distal to the site of an injury with traumatic transection of a peripheral nerve. In this distal nerve segment in longitudinal section, small axonal and myelin fragments lie within myelin ovoids as vacuolar digestion chambers (▲). Regeneration is possible because the proximal nerve stump undergoes axonal sprouting, and Schwann cells proliferate to remyelinate the nerve fiber. Regeneration proceeds along the course of the degenerated axon at a rate of approximately 2 mm/day.
Traumatic neuroma . This unorganised jumble of sprouding neurits or axons in bundles have
This disorganized jumble of sprouting neurites, or axons in bundles (♦) have become embedded within a dense reactive connective tissue stroma. This nonneoplastic lesion occurs when a peripheral nerve is severed or damaged, and the proximal axons try to regrow, but are unable to connect with the distal axonal sheaths, forming the haphazard mass of nerve and fibrous connective tissues. The result can become a painful nodule. A common location for this lesion is between the bases of the second and third digits of the foot because a characteristic human folly is fashion over function, with choice of footwear such as pointed-toe shoes and high heels that produce compression injury.
A 36 year old man is admitted to accident and emergency with a neck/spinal injury following a motor cycle accident. Upon examination he is able to feel pain in his left arm and leg, but not his right arm and leg, and touch only in his left leg, and not in his right. He also has right-sided hemiparesis.
What can you deduce about the condition of his spinal cord?
