By T. Kayor. Knox Theological Seminary.
The skin and neural tissue arise from a single become the motor neurons that control muscles order 17.5 mg lisinopril. An even lower layer cheap 17.5 mg lisinopril free shipping, known as the ectoderm generic lisinopril 17.5mg with visa, in response to signals provided concentration promotes the formation of interneurons that by an adjacent layer, known as the mesoderm. A number of molecules interact to determine whether the A combination of signals also determines the type of chem- ectoderm becomes neural tissue or develops in another way to ical messages, or neurotransmitters, that a neuron will use to become skin. Studies of spinal cord development in frogs show communicate with other cells. For some, such as motor neu- that one major mechanism depends on speciﬁc molecules that rons, the choice is invariant, but for others it is a matter of inhibit the activity of various proteins. Scientists found that when certain neurons are main- activity of such proteins, the tissue becomes skin. If other mol- tained in a dish without any other cell type, they produce the ecules, which are secreted from mesodermal tissue, block pro- neurotransmitter norepinephrine. In contrast, if the same neu- tein signaling, then the tissue becomes neural. The mature nervous system production of these molecules, it is the turning on of a partic- contains a vast array of cell types, which can be divided into two ular set of genes that begins the production of speciﬁc neuro- main categories: the neurons, primarily responsible for signal- transmitters. Many researchers believe that the signal to engage ing, and supporting cells called glial cells. For As neurons are produced, they move from the neural tube’s example, a key factor in spinal cord development is a secreted ventricular zone, or inner surface, to near the border of the mar- protein called sonic hedgehog that is similar to a signaling pro- ginal zone, or the outer surface. The protein, initially secreted from meso- they form an intermediate zone where they gradually accumu- dermal tissue lying beneath the developing spinal cord, marks late as the brain develops. Cells further away are exposed to brain, but is particularly prominent in the formation of a large lower concentrations of sonic hedgehog protein, and they cerebral cortex in primates, including humans. A cross- sectional view of the occipital Outer surface lobe (which processes vision) of Fetal a three-month-old monkey fetus monkey brain brain (center) shows immature neurons migrating along glial fibers. These neurons make Migrating neuron transient connections with other neurons before reaching their destination. A single migrating neuron, shown about 2,500 Migrating times its actual size (right), uses zone a glial fiber as a guiding sca≈old. To move, it needs ad- hesion molecules, which recog- Glial nize the pathway, and contrac- ﬁber tile proteins to propel it along. Inner surface 9 neurons slither from the place of origin near the ventricular sur- corresponding, and again related, human receptors. Proper neuron migration requires multiple mech- permit electric signals in the axon to jump to the next cell, where anisms, including the recognition of the proper path and the they can either provoke or prevent the generation of a new sig- ability to move long distances. The regulation of this transmission at synapses, and the inte- distance migration is the movement of neurons along elongated gration of inputs from the thousands of synapses each neuron ﬁbers that form transient scaffolding in the fetal brain. Many receives, are responsible for the astounding information- external forces, such as alcohol, cocaine or radiation, prevent processing capabilities of the brain. For processing to occur prop- proper neuronal migration and result in misplacement of cells, erly, the connections must be highly speciﬁc. Some speciﬁcity which may lead to mental retardation and epilepsy. Further- arises from the mechanisms that guide each axon to its proper more, mutations in genes that regulate migration have recently target area. Additional molecules mediate “target recognition” been shown to cause some rare genetic forms of retardation and whereby the axon chooses the proper neuron, and often the epilepsy in humans. Few of Once the neurons reach their ﬁnal location, they must make these molecules have been identiﬁed. There has been more suc- the proper connections for a particular function, such as vision cess, however, in identifying the ways in which the synapse forms or hearing, to occur. The tiny portion of the axon stalk-like appendages can stretch out a thousand times longer that contacts the dendrite becomes specialized for the release of than the cell body from which they arise. The journey of most neurotransmitters, and the tiny portion of the dendrite that axons ends when they meet the branching areas, called den- receives the contact becomes specialized to receive and respond drites, on other neurons. Special molecules pass between the sending and at a considerable distance, sometimes at opposite sides of the receiving cell to ensure that the contact is formed properly. In the case of a motor neuron, the axon may travel from the spinal cord all the way down to a foot muscle. The linkup Paring back sites, called synapses, are where messages are transferred from Following the period of growth, the network is pared back to one neuron in a circuit to the next.
May resemble AIDP lisinopril 17.5mg without a prescription, and proceed to lethargy purchase 17.5 mg lisinopril amex, coma lisinopril 17.5 mg on-line, and death. A one week or longer exposure at lesser doses causes neuropathy with alope- cia, hyperkeratosis, Mee’s lines, ataxia, chorea, CNS palsies, autonomic dys- function with tachycardia. Chronic exposure at low levels causes extrapyramidal dysfunction and ques- tionable sensorimotor neuropathy. Thallium is found in rodenticides and insecticides, and may be ingested in Pathogenesis situations of homicide and suicide. Diagnosis made by detection of thallium in urine or Diagnosis organs. Potassium chloride or Prussian blue is used for treatment, but efficacy is Therapy questionable. Recovery begins six months following discontinuation of exposure, and recov- Prognosis ery for subacute cases is good. In: Dyck PJ, Thomas PK, Griffin JW, Low PA, Reference Poduslo JF (eds) Peripheral neuropathy, 3rd edn. Saunders, p 1549–1570 324 Hereditary neuropathies Hereditary motor and sensory neuropathy type 1 (Charcot-Marie-Tooth disease type 1, CMT) Genetic testing NCV/EMG Laboratory Imaging Biopsy ++ ++ ++ Fig. Sural nerve biopsy from a patient with HMSNIII (De- jerine-Sottas disease). The biop- sy shows evidence of severe de- myelination with thinly myeli- nated fibers and formation of multiple onion bulbs (black ar- rows) Fig. C and D Atrophic lower legs with foot deformity Fig. Onion bulb for- mation in a nerve biopsy (ar- rows) CMT type 1 typically results in loss of peripheral nervous system myelin. Anatomy/distribution Usually within the first or second decade of life, patients experience mild distal Symptoms sensory loss and more severe distal weakness. Pes cavus and hammer toes, the characteristic foot deformity of CMT, usually Clinical syndrome/ appears in early childhood (Fig. Anterior leg compartment muscles be- signs come weak and atrophy over time, leading to foot drop (Fig. Wasting may be seen in the intrinsic hand muscles in severe cases (Fig. Areflexia is more pronounced distally, but may be noted in the upper extremities. Peripheral nerves, especially the greater auricular and brachial plexus, become thick and palpable. Trisomy 17 has been documented in some rare cases, and is accompanied by a spectrum of developmental abnormalities. Point muta- tions in the genes for the myelin protein Po (CMT-1B) and the transcription factor EGR-2 (CMT-1D) also cause CMT type 1. The various forms of CMT-1 have the same clinical presenta- tion. Diagnosis Motor and sensory nerve conduction velocities are uniformly slowed in all four limbs. Biopsy shows onion bulb formation, suggesting demyelination (Fig. Genetic testing can be done to identify the responsible mutation. Family members should also be tested to identify carriers. Differential diagnosis Other inherited neurologic disorders that present in the early decades of life should be considered. The spinocerebellar ataxias and leukodystrophies can be distinguished by the presence of cranial nerve, cerebellar, and long tract signs that are not found in CMT. HNPP may resemble CMT, but the history of pressure palsies and extremely disproportionate distal latencies, in comparison to almost normal NCVs, will indicate HNPP. Electrodiagnostic studies are usually asym- metric in inflammatory neuropathies. Finally, inherited myopathies and spinomuscular atrophy show no impairment of sen- sory function on examination.
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