By A. Hjalte. Midwestern Baptist College. 2018.

Because neurons show little 100mg penegra with mastercard, if any order penegra 100mg line, capacity to re- rotrophins (e order 50mg penegra mastercard. Intravenous injec- The factor called Nogo is an example discount penegra 100 mg visa. Successfully transplanted donor duces swelling at the site of injury and improves recovery buy penegra 50mg without a prescription. Spinal tains the cell bodies of the sensory neurons. A ganglion cord tumors are diagnosed by magnetic resonance imag- (GANG-le-on) is any collection of nerve cell bodies lo- ing (MRI) or other imaging techniques, and treatment is cated outside the CNS. Fibers from sensory receptors 9 by surgery and radiation. The ventral roots of the spinal nerves are a combina- Injuries Injury to the spinal cord may result from tion of motor (efferent) fibers that supply muscles and wounds, fracture or dislocation of the vertebrae, hernia- glands (effectors). The cell bodies of these neurons are lo- tion of intervertebral disks, or tumors. The most common cated in the ventral gray matter (ventral horns) of the causes of accidental injury to the cord are motor vehicle cord. Because the dorsal (sensory) and ventral (motor) accidents, falls, sports injuries (especially diving acci- roots are combined to form the spinal nerve, all spinal dents), and job-related injuries. Branches of the Spinal Nerves Damage to the cord may cause paralysis or loss of sen- Each spinal nerve continues only a short distance away sation in structures supplied by nerves below the level of from the spinal cord and then branches into small poste- injury. Different degrees of loss are named using the root rior divisions and larger anterior divisions. The larger an- -plegia, meaning “paralysis,” for example: terior branches interlace to form networks called plexuses (PLEK-sus-eze), which then distribute branches ◗ Monoplegia (mon-o-PLE-je-ah)—paralysis of one limb to all parts of the body (see Fig. The three main ◗ Diplegia (di-PLE-je-ah)—paralysis of both upper or plexuses are described as follows: both lower limbs ◗ Paraplegia (par-ah-PLE-je-ah)—paralysis of both lower ◗ The cervical plexus supplies motor impulses to the limbs muscles of the neck and receives sensory impulses from ◗ Hemiplegia (hem-e-PLE-je-ah)—paralysis of one side the neck and the back of the head. The phrenic nerve, of the body which activates the diaphragm, arises from this plexus. Box 9-1, Spinal Cord Injury: Crossing the Divide, con- ◗ The lumbosacral (lum-bo-SA-kral) plexus supplies tains information on treatment of these injuries. The largest branch in this plexus is the sciatic (si-AT-ik) nerve, which leaves the dorsal part of the pelvis, passes beneath the gluteus ◗ The Spinal Nerves maximus muscle, and extends down the back of the There are 31 pairs of spinal nerves, each pair numbered thigh. At its beginning, it is nearly 1 inch thick, but it according to the level of the spinal cord from which it soon branches to the thigh muscles; near the knee, it arises (see Fig. Each nerve is attached to the spinal forms two subdivisions that supply the leg and the foot. On each dorsal root is a marked swelling Dermatomes Sensory neurons from all over the skin, of gray matter called the dorsal root ganglion, which con- except for the skin of the face and scalp, feed information 192 CHAPTER NINE C-2 extremities. It affects both sensory and C-2 motor function, causing symptoms of pain and paralysis. Causes include C-3 chronic intoxication (alcohol, lead, C-3 C-4 drugs), infectious diseases (meningitis), C-4 C-5 metabolic diseases (diabetes, gout), or T-2 C-6 nutritional diseases (vitamin deficiency, C-5 T-3 T-2 T-6 T-3 starvation). Identification and treatment T-4 T-5 T-7 of the underlying disorder is most im- T-6 T-8 C-7 T-9 portant. Because peripheral neuritis is a T-7 T-1 T-8 T-10 symptom rather than a disease, a com- T-11 C-8 T-9 plete physical examination may be C-6 T-10 T-12 T-1 T-11 needed to establish its cause. T-12 C-6 Sciatica (si-AT-ih-kah) is a form of C-7 L-1 L-1 L-1 S-3 L-1 peripheral neuritis characterized by severe pain along the sciatic nerve and S-3 S-3 its branches. The most common L-2 L-2 causes of this disorder are rupture of a S-4 C-8 L-2 L-2 disk between the lower lumbar verte- brae and arthritis of the lower part of L-3 L-3 the spinal column. Herpes zoster, commonly known S-2 S-2 as shingles, is characterized by numer- L-5 L-5 L-4 ous blisters along the course of certain L-4 L-4 nerves, most commonly the intercostal L-5 nerves, which are branches of the tho- racic spinal nerves in the waist area. It is caused by a reactivation of a prior S-1 S-1 S-1 infection by the chickenpox virus and involves an attack on the sensory cell Anterior view Posterior view bodies inside the spinal ganglia. Initial symptoms include fever and pain, fol- Figure 9-15 Dermatomes. A dermatome is a region of the skin supplied by a sin- lowed in 2 to 4 weeks by the appear- gle spinal nerve. ZOOMING IN Which spinal nerves carry impulses from the skin of ance of vesicles (fluid-filled skin le- the toes? The drainage from these vesicles contains highly contagious liquid. The neuralgic pains may persist into the spinal cord through the spinal nerves.

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This was later found to be due to its þ oxidative byproduct 1-methyl-4-phenylpyridinium ion (MPP ) buy penegra 50 mg lowest price. Others have demonstrated MPTP’s toxic properties on dopaminergic neurons (15) cheap penegra 50mg with mastercard. MAO-B inhibitors were originally thought to prevent this conversion via MAO inhibition buy discount penegra 50 mg line. Since then cheap penegra 100mg amex, MPTP has been shown to inhibit mitochondrial respiration via complex I buy penegra 50mg fast delivery, through free radical synthesis (18). Matsubara and others (20) showed selegiline prevented mitochondrial toxicity elicited by þ MPTP and 2,9-Me2NH , which is an N-methylated b-carbolinium cation and an analog of MPTP with protoxic activity. They hypothesized that selegiline impacts mitochondrial electron transport, resulting in membrane potential stabilization. Tatton and Greenwood (21) exposed rats to MPTP for 72 hours. These rats were sacrificed and the substantia nigra compacta stained with tyrosine hydroxylase (TH þ) immunostain to measure the amount of dopaminergic cells. Selegiline was shown to prevent 50% of the loss due to MPTP. The importance of this observation was the absence of MAO-B activity in those regions implying a different mechanism for selegiline’s action. DSP-4 is a neurotoxin that inhibits H-noradrenaline uptake into central and peripheral noradrenergic neurons in rodents. Knoll (23) found that selegiline could protect striatal dopaminergic cells from 6- hydroxydopamine (6-OHDA) neurotoxicity. These studies suggest that MAO-B inhibitors may have other neuroprotective properties besides that of MAO inhibition. Increased GFAP expression contributes to tissue scarring and creates a physical barrier near damaged neurons. Presumably, MAO-B inhibitors either inhibit the physical barrier, prohibiting vital repairs to damaged neurons, or they protect neurons from damage directly, thus producing less GFAP expression. In this study, selegiline induced new protein synthesis. These experiments give credence to neuronal protection. The possible mechanisms include direct neuronal survival, regeneration, or indirect induction of cellular changes. BIOCHEMICAL PROPERTIES Selegiline is a selective irreversible MAO-B inhibitor. Taken orally, it is readily absorbed from the intestine and reaches plasma levels in 30–120 minutes. Its major metabolites, L- methamphetamine and L-amphetamine, have half-lives of 20. At doses of 5 and 10 mg it has mild antiparkinsonian effects without causing pressor effects. At higher doses such as 30 and 60 mg it has greater antidepressant effects but is associated with an increased pressor effect via tyramine, requiring patients to adhere to a low-tyramine diet. It has an extremely long half-life as confirmed with positron emission tomography (PET) imaging (27,28). Withdrawal from selegiline is not associated with an amphetamine-like withdrawal. Selegiline also signifi- cantly increases phenylethylamine (PEA) output. PEA is a strong dopamine uptake inhibitor and induces dopamine release (29). CLINICAL APPLICATIONS Selegiline is primarily used in patients with early PD as monotherapy or as adjunctive therapy to levodopa. It is usually used as 5 mg every morning or 5 mg twice a day, in the morning and afternoon. It is not given at night to avoid insomnia from methamphetamine metabolites. The Quality Standards Subcommittee of the American Academy of Neurology (32) confirmed that selegiline has only mild symptomatic antiparkinsonian effects when used as monotherapy. Compared to placebo, selegiline improves motor scores in PD patients (33–35).

Almost all patients are relatively cation of Winters et al generic penegra 50 mg with visa. This classification divides hemiplegic which is then helpful for planning treatment discount penegra 50mg visa. Transverse rotational plane malalignments do not fit into this classification and should be seen as an additional problem best penegra 100 mg. Her main complaint was that she could not lift her foot penegra 50 mg with amex. Physical examination of her right ankle demonstrated an active toe extensor cheap 100 mg penegra visa, and some apparent activity of the tibialis anterior on withdrawal stimulus of a pin stick on the sole. Ankle dorsiflexion was 10° with knee flexion and 20° with knee extension. Ankle kinematics showed no active dorsiflexion in swing phase and no EMG activity of the tibialis anterior (Figure C7. Observation of her gait demonstrated an extended hallux in swing phase, but no apparent dorsiflexion was in swing phase. She was ordered a leaf-spring AFO that worked well when it was worn. Type 1 has ankle plantar flexion in swing phase with an inactive or very weak tibialis anterior, which is the cause of the plantar flexion. Type 2 has an equinus gait pattern but with spastic or contracted plantar flexors, which overpower an active dorsiflexor. Type 3 includes the ankle position of type 2, further adding abnormal function of the knee joint. Type 4 includes all problems of type 3 with the addition of abnormal function of the hip joint muscles. The separation of these types is usually easy through a combination of physical examination, EMG, kinematic evaluation, and ki- netic data. As with all biological groups, however, there are intermediate pa- tients. This system does not consider transverse plane deformities; however, most children with significant residual internal femoral torsion are types 3 or 4, and tibial torsion occurs with types 2, 3, or 4. Type 1 In children with hemiplegic pattern CP, type 1 is the least common pattern of involvement. Type 1 occurs more with adult stroke or with a peripheral nerve injury. If this type is identified in a child with CP, the physical exami- nation will demonstrate full passive dorsiflexion; however, no active dorsi- flexion can be demonstrated. The kinematic examination will show plantar flexion at initial contact and no dorsiflexion in swing phase. The EMG will demonstrate a tibialis anterior that is silent or nearly silent. The primary treat- ment for type 1 hemiplegia is a relatively flexible leaf-spring AFO (Case 7. In very rare situations where the tibialis posterior has normal tone and normal phasic firing, the tibialis posterior can be transferred through the interosseous membrane to the dorsum of the foot. However, this transfer is mainly used with peripheral nerve palsy. With central lesions, relearning is difficult as this is an out-of-phase transfer, and transfer of the spastic tibialis posterior leads to very severe foot deformities. Gait 345 Type 2 The most common subtype of hemiplegia is type 2, making up approximately 75% of all children with hemiplegia. Typically, children learn to walk inde- pendently between 15 and 20 months of age, either with toe walking or foot flat with a planovalgus. The early treatment is to provide the children sup- port through the use of an orthotic, usually starting with a solid ankle AFO, then following with an articulated AFO for the second orthotic. If a child has a very spastic gastrocsoleus, botulinum toxin injection for two or three cycles can help parents apply the AFO and make AFO wear more comfortable for the child.

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Although early studies examining outcomes after thalamotomy reported decrements in language and memory with regularity (see Ref order penegra 100mg free shipping. Initial reports of the apparent cognitive safety of subthalamotomy (128 discount 100mg penegra visa,129) remain to be confirmed by larger discount 50mg penegra mastercard, controlled studies best 50 mg penegra. Deep Brain Stimulation Nonablative surgical procedures for the treatment of PD involve either unilateral or bilateral implantation of high-frequency stimulation electrodes into deep brain nuclei penegra 100 mg fast delivery. Studies detailing neuropsychological outcomes after unilateral pallidal (GPi) deep brain stimulation (DBS) have supported the neurobehavioral safety of this technique (see Refs. The majority of studies indicate that even bilateral GPi stimulation is cognitively well tolerated (134–136), although in isolated cases cognitive declines can occur (125,137). There remain few studies evaluating cognitive outcomes after thalamic DBS, but preliminary findings suggest that this procedure is associated with minimal cognitive morbidity soon after (138,139) and up to one year after surgery (140). Indeed, subtle and limited cognitive improvements might be witnessed after thalamic DBS. The majority of DBS procedures now target the subthalamic nucleus (STN). Modest decrements in verbal fluency are the most commonly reported adverse cognitive sequelae associated with STN DBS. Findings regarding possible postoperative declines and/or improvements in global cognitive abilities, memory, attention, and executive functions are incon- sistent (see Refs. When considered in the context of the considerable benefits of surgery on motor functions, mood state, and quality of life (142), the cost of possible minor and/or transient cognitive declines in a minority of well-selected patients seems to be overshadowed by the benefits. Preliminary evidence indicates that elderly patients (>69 years), as well as those patients displaying presurgical cognitive deficits, might be at greater risk for neurobehavioral morbidity after STN DBS. Transplantation Fetal mesencephalic tissue transplantation studies have indicated variability in neurocognitive outcomes among individual patients, but given small sample sizes, the source of variability is difficult to identify (see Ref. NEUROPSYCHOLOGICAL ASPECTS OF PARKINSON-PLUS SYNDROMES AND ESSENTIAL TREMOR ‘‘Parkinson-plus syndromes’’ traditionally include progressive supranuclear palsy (PSP), multiple system atrophy (MSA), and corticobasal ganglionic degeneration (CBGD). Although sparse, preliminary neuropsychological studies indicate that the cognitive impairment profiles likely differ across the parkinson-plus syndromes (see Ref. A summary of key differences is presented in Table 4. Progressive Supranuclear Palsy Prevalence rates of dementia in PSP range between 50 and 80%, although some authors contend that these numbers reflect overdiagnosis due to bradyphrenia, emotional problems, and visual dysfunction that accompany PSP. Cognitive deficits are seen in approximately 50% of patients with PSP (143), with the neuropsychological profile in PSP being typical of diseases with subcortical involvement, including slowed information processing, executive dysfunction, and information-retrieval deficits (144). As compared to patients with PD, cognitive slowing and executive dysfunction in PSP emerge earlier in the disease course, are more severe, and progress more rapidly (145–148), and this differential executive dysfunction may reflect radiographically demonstrated differences in frontal atrophy between the Copyright 2003 by Marcel Dekker, Inc. Executive dysfunction in PSP may also differ qualitatively from that in PD (150). Memory and attention are relatively intact in PSP, although retrieval deficits and accelerated rates of forgetting may be present (151,152). The early presence of cognitive impairment distinguishes PSP from MSA (153). Multiple System Atrophies The MSA nomenclature includes several different diseases, including olivopontocerebellar atrophy (OPCA), striatonigral degeneration (SND), and Shy-Drager syndrome (SDS). Cognitive deficits are relatively mild in most forms of MSA, and dementia is not a common feature of these conditions (154), except perhaps in OPCA, in which 40–60% of patients may develop dementia, with dementia prevalence greater in familial forms of the Copyright 2003 by Marcel Dekker, Inc. Mild executive and memory deficits have been reported in MSA (SND and SDS) (156) but are considered to be of similar severity to those observed in nondemented patients with PD (147,157). Patients with MSA may show more pronounced attentional impairments and longer reaction times than patients with PD (157,158). Corticobasal Ganglionic Degeneration The prevalence of cognitive impairment and/or dementia in CBGD is not established. Neuropsychological functions appear to be relatively preserved in the early stages of CBGD (at least within an average of 5 years of diagnosis (159), with dementia emerging as a more common feature later in the disease course (160). While the neuropsychological profile of CBGD reveals both cortical and subcortical features (161), it is possible to differentiate CBGD from AD and PSP at the group level (147,162). The neuropsychological profile associated with CBGD is marked by significant executive dysfunction, which is comparable in severity to PSP, but relatively milder than is observed in patients with AD.

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