What is Parkinsons Disease
The in vitro and in vivo (in man) iontophoresis of the anti-Parkinson's drug apomorphine has been studied (79,80). In vivo, after one-hour iontophoresis, plasma profiles comparable to a zero-order infusion study were obtained, although the concentrations were subtherapeutic. Deconvolution of the data demonstrated that a steady iontophoretic flux was attained following only 10 to 20 minutes of iontophoresis. Plasma levels decreased rapidly following current interruption. Minor skin irritation and tingling sensations were reported. The feasibility of iontophoretically administering therapeutic doses of ropinirole has also been shown in vitro (23).
Wolff-Parkinson-White syndrome is the result of a congenital accessory pathway to the ventricles that bypasses the AV node, resulting in preexcitation of the ventricles. The impulse still goes down through the AV node normally, but also goes down the accessory pathway, which conducts much faster than the AV node. The result is that the impulse gets to the ventricles early via the accessory pathway, producing an early slurred upstroke of the R wave called a delta wave (Figure 2.4).
As time has progressed, the GnRH agonists have also been shown to have side effects. These include memory loss, parkinsonism, anemia, and osteoporosis, in addition to the hot flushes and impotence that were obvious from their first use. The most important of the side effects phys
Decreased dopamine concentration in substantia nigra, locus ceruleus, and striatum ( LENTICULAR AND CAUDATE NUCLEI) i n tracy to p I as m i c inclusion bodies ( LfAXT BODIF.S) in substantia nigra. Bromocriptine (dopamine agonist), anticholinergics, levodopa to produce dopamine), selegiline (sclcctivc MAO-B enzyme inhibitor). Also called paralysis agitans, it is an idiopathic disorder with a male predominance characterized by decreased dopamine due to basal ganglia degeneration, mainly in the substantia nigra, with a resultant relative excess of acetylcholine. Since dopamine cannot cross the blood-brain barrier, levodopa, a dopamine precursor, is given levodopa crosses the blood-brain barrier and is converted to dopamine in the brain.
In addition to the possible treatment of genetic defects, virus vectors may also be useful for the treatment of a number of acquired diseases. These include cancer, HIV infection, Parkinson's disease, injuries to the spinal cord, and vascular diseases such as restenosis and arteriosclerosis. A partial listing of candidate diseases for gene therapy is given in Table 9.1.
In humans, AD displays a protracted clinical course covering 10-20 years. The life span of laboratory mice does not exceed much more than approx. 2 years, and it is surprising that the entire pathologic history of the disease can be compressed into 6-12 months. It is evident that this shorter time span presents a great opportunity and considerable advantages for investigations into the pathogenesis of the devastating neurodegeneration of AD, particularly to identify new methods for early and objective diagnosis and to test novel therapeutic drugs or strategies. Experiments and trials could be measured in months in transgenic mice, as opposed to years in humans. As these and other transgenic models are available, there is every reason to believe that they will help to accelerate the pace of drug discovery, leading to the recognition of therapeutic agents that are effective in postponing the onset or slowing the progression of neurodegenerative diseases, not only Alzheimer's disease,...
Functionality of antigen-specific CTL was observed. In a chronic-infection mouse model of LCMV, one highly invasive lab-derived LCMV clone will cause prolonged infection with detectable viremia in blood and multiple peripheral organs. PD-1 was dramatically upregulated on CTL in response to the viral infection, and its expression was maintained during chronic infection, while B7-H1 is persistently expressed on spleen cells. These infected mice have not only a significant decrease in the number of antigen-specific memory CD8 T-cell population, but also a functional impairment of their remaining memory T cells. Interestingly, blockade of B7-H1 PD-1 pathway by monoclonal antibodies against B7-H1 or PD-1 increased proliferation of several virus-specific CTL clones, restored CTL function and reduced viral burden (Barber et al.,2006). More importantly, persistent upregulation of PD-1 is also observed on HIV, HCV and HBV viral-specific CTLs in chronically infected patients and correlates with...
Additionally, Parkinson patients also benefit from the low-leucine vegan diet because the low-leucine intake decreases the competition with their oral DOPA intake, so they can use lower amounts of DOPA medication to suppress their Parkinson disease symptoms without undesirable side effects from the higher DOPA intake.35
Berke GS, Gerratt B, Kreiman J, Jackson K (1999) Treatment of Parkinson hypophonia with percutaneous collagen augmentation. Laryngoscope 109 1295-1299 12. Kim SH, Kearney JJ, Atkins JP (2002) Percutaneous laryngeal collagen augmentation for treatment of parkinsonian hypophonia. Otolaryngol HeadNeck Surgi26 653-656
Dopaminergic neurons in the substantia nigra in the midbrain project to the striatum. The effect of dopamine excites or drives the direct pathway, increasing cortical excitation. Dopamine excites the direct pathway through D( receptors and inhibits the indirect pathway through D2 receptors. Parkinsonism pill-rolling tremor of the fingers at rest, lead-pipe rigidity, and akinesia Degeneration of the substantia nigra Lesions of the direct pathway result in an underactive cortex and hypokinetic disturbances in which there is a slowing or absence of spontaneous movements. The best known disorder of the direct pathway is caused by the degeneration of dopaminergic neurons of the substantia nigra in Parkinson disease. Because the cortex is underactive, Parkinson patients have problems initiating movements, combined with a reduction in the velocity and amplitude of the movements. The tremor at rest is the classic pill rolling tremor seen in the fingers. Skeletal muscles in the upper limbs...
Patients 4 , in 38 of those with cancer 5 , in 47 of those with stroke 6 , in 45 of those with myocardial infarction (7), and in 39 of those with Parkinson's disease 8 . Thus, underrecognizing, underdiagnosing and undertreating depressive disorder is an ethical issue facing the medical profession.
Multiple sclerosis and Parkinson's disease are associated with abnormal latency periods. Lesions of the optic nerve, optic tract, and cerebral cortex visual center(s) can be identified with a visual-evoked response exam. Visual field defects due to retinal damage, macular degeneration, and glaucoma may be detected by VER.
Have been mobile (e.g., vocal fold paresis senile atrophy). We routinely inject both vocal folds at the same time, if necessary. Even when injecting a paralyzed vocal fold, we often inject a mobile contralateral vocal fold if it is bowed and atrophic. Our indications for injection augmentation with CaHA are presented in Table 8.4.1. We have performed bilateral injections in 13 individuals with glottal insufficiency secondary to Parkinson's hypophonia. Our results have been extremely positive and appear to be similar to the degree of improvement reported by other investigators with collagen augmentation 11,12 .
Generally the fear is that their hands or heads might shake social phobics rarely actually tremble or shake so that they write with a scrawl, rattle their coffee cup against the saucer, spill soup when raising their spoon to their lips, or nod their head visibly when talking. This contrasts strikingly with sufferers from brain diseases which actually cause obvious shaking. People with Parkinson's disease, for example, do not fear doing things in public despite the shaking of their head and hands. Similarly, fear of blushing,
The mesencephalon (midbrain) contains the substantia nigra, which is the location of the degenerating dopaminergic neurons in Parkinson disease. 2. Answer E. In Parkinson disease, loss of dopamine enhances the effects of the indirect basal ganglia pathway, which is also driven by cholinergic neurons intrinsic to the striatum. A muscarinic blocker will reduce the stimulatory effects of ACh on the indirect pathway.
Any medication with an anticholinergic effect (see Table 21.1), including antispasmodics, antihistamines, antipsychotics, antidepressants, and anti-parkinsonian drugs, can induce urinary retention and overflow incontinence. Diuretics, and caffeine and alcohol through their diuretic effects, can increase urine flow and induce or worsen any form of incontinence. Sedatives, antipsychotics, and alcohol can cause sedation, worsening the woman's ability to respond to urinary urges.
HPI The patient also states he has been having palpitations and insomnia He suffers from Parkinson's disease and has been taking levodopa for a long time. PE VS tachycardia (HR 1 15) postural hypotension. PE patient thin typical parkinsonian gait masklike fades pill-rolling tremor of hands choreiform movements of head and hands grimacing facial movements. Treatment Minimize side effects by taking drug with meals or in smaller doses. Often, administration of carbidopa diminishes side effects. Tolerance to emetic effect may also develop. Antiemetics may be given, but these may reduce antiparkinsonian effects. levodopa, a precursor of dopamine, does. When this drug is administered, it is usually given in combination with carbidopa, an inhibitor of the peripheral dopa decarboxylase (thus increasing the half-life and plasma levels of levodopa). Dyskinesias are a common side effect, as are GI symptoms (nausea and vomiting) and postural hypotension. Arrhythmias, anxiety, depression,...
Either traumatic brain injury or dopamine-active medications commonly cause abnormal involuntary movements (AIMS) following trauma. Traumatic brain injury, particularly injury to the basal ganglia, can produce dystonia, dyskinesia, choreoathetosis, ballismus, myoclonus, asterixis, or Parkinsonism.69-80 Dystonia is an involuntary sustained contraction of both agonist and antagonist muscles. It may cause repetitive, twisting movements or abnormal postures.69,70 The psychiatrist or neurologist will be familiar with this disorder, as it frequently is caused by high-potency neuroleptic medicines such as haloperidol or fluphenazine. Dystonia generally has two causes following brain trauma injury to the basal ganglia or as a side effect of neuroleptic medications. Dyskinesias are stereotyped, automatic movements of the limbs or oral-facial muscles, and they may also result from injury to the basal ganglia or from neuroleptic medication side effects. Choreoathetosis (choreo dance, athetosis...
Permeability coefficients have been measured for chemicals that exhibit diverse ionization behavior. Many compounds are essentially nonionized at the pH of the experiment (i.e., typically 2 pH 10). However, many others (e.g., aniline, caffeine, codeine, isoquinoline, ibuprofen, and nicotine among others) exist in equilibrium with a charged species (frequently protonated amines or dissociated carboxylic acid). Some compounds are always completely ionized (e.g., paraquat or tetraethylammonium bromide). Others are zwitterionic (i.e., net neutral) but never nonionized (e.g., 5-fluorouracil). Still others coexist as a complex mixture of zwitterionic, charged, and nonionized species (e.g., 2-amino-4-nitrophenol, dopamine, hydromorphone, isoprenaline, levodopa, morphine, and nicotinic acid). The relative rates of penetration of anionic, cationic, and zwitterionic species are not precisely known. Sznitowska and colleagues have measured the penetration of net anionic, cationic, and...
Voiding is coordinated by the neurons of the pontine-mesencephalic gray matter or the Pontine Micturition Center (PMC) (17,18). Voiding depends on the spinobulbospinal reflex through the PMC after receiving input from the hypothalmus, thalmus, basal ganglia cerebellum, and cerebral cortex. The input from the suprapontine center is predominantly inhibitory but may have partial facilitory action. The major inhibitory areas appear to be the cerebellum, basal ganglia, and cerebral cortex, while facilitation may be regulated by the posterior hypothalmus and anterior pons (17-23). Additionally, most of the suprapontine input into the PMC is inhibitory. Interruption of this input by a cerebrovascular accident, Parkinson's disease, or brain tumor may result in detrusor overactivity or detrusor hyperreflexia (DH). This detrusor hyperreflexia may manifest itself with symptomatic frequency, urgency, and urge incontinence.
Similar tau pathology is evident in conditions known as familial multiple system tauopathy with presenile dementia (MSTD) (25) and disinhibition-dementia- parkinsonism-amyotrophy complex (DDPAC) (21,26), two tauopa-thies with an intronic mutation in the tau gene. In MSTD, the established preponderance of four-repeat protein tau isoforms causes axonal swellings in the spinal cord, as observed in the htau40 mice, as well as NFTs in the brain and spinal cord. In DDPAC, excess of four-repeat protein tau provokes anterior horn pathology with muscle wasting, in the absence of NFTs. Subtle regional differences in expression and sensitivity of neurons to different isoforms of protein tau are thought to be involved in the differential aspects of pathology. This subtlety needs further experimental clarification in vivo, probably by making use of other gene promoters or control elements.
The most direct indication of the pathophysiology caused by protein tau is the mutations in the tau gene that are linked to neurodegeneration and dementia, known as frontotemporal dementia with parkinsonism linked to chromosome 17 (FTDP-17) (2). In vitro, most clinical missense mutations located in the microtubule binding domains reduce the association of protein tau with microtubuli (21). In addition, several intronic mutations as well as two missense mutations induce a preponderance of four-repeat over three-repeat protein tau isoforms (2). All patients carrying these mutations develop protein tau filaments in their brain consisting of hyperphosphorylated protein tau. Although mutations in tau do not segregate with AD, the resemblance of clinical symptoms (i.e., dementia) and pathology (i.e., NFTs) in AD and FTDP-17 patients will help to elucidate the etiology of the tauopathy in AD.
Perioperative monitoring of left ventricular function is particularly important in patients with poor left ventricular function, who undergo a valve repair or replacement combined with myocardial revascularisation27'28. New segmental wall motion abnormalities have been shown to occur within seconds after the onset of regional ischemia29 and is more sensitive than electrocardiographic and hemodynamic monitoring30. Echocardiographic evidence of ischemia has a close relation with postoperative outcome30. Regional left ventricular function and regional wall motion can be scored with a segmental wall-motion scoring system that is also used for transthoracic echocardiography (table 1). If all wall segments are visible, this scoring system uses the sum of scores of all segments divided by the total number of segments. A wall motion score 1 is an indication of left ventricular dysfunction. It is important to remember, that myocardial ischemia is not the only cause of regional myocardial...
Extrapyramidal acute dystonia dyskinesia akathisia parkinsonism tardive dyskinesia dystonia (akathisia) Anticholinergic dry mouth constipation blurred vision urinary retention sexual dysfunctions Ophthalmologic lenticular changes pigmentary retinopathy Many side effects can successfully be managed by dose reduction or switching from one drug to another 68 . So far specific pharmacologic interventions are only successful against EPS. Even though the efficacy of anticholinergics against acute dystonia or parkinsonism 69 and that of beta-blockers in treating akathisia 70 are impressive, these drugs should be used cautiously. Anticholinergics are potent psychotropic drugs 71 that may lead to memory deficits 72 , substance abuse 73 , as well as to a worsening of psychotic symptoms 74 . Therefore, the general prophylactic use of anticholinergic drugs is discouraged, a position also fortified by a World Health Organization (WHO) recommendation 75 . The exception to this rule are patients...
For this diagnosis, the mood disorder must be integral to the medical condition, perhaps even sharing the pathophysiology. Depressive symptoms can be part of many medical conditions that are common in middle-aged women (Table 7.4) and sometimes are the presenting symptoms of a condition. Up to one-third of cancer survivors and their family members suffer from depression,34 and at least half of patients with epilepsy or Parkinson's disease have depression.35 Management consists primarily of treating the medical condition, but specific treatment of depressive symptoms may also be necessary.
Induced Parkinson's syndrome aside from discontinuation of offending drug. Discussion Several drugs may produce Parkinson-like symptoms, including haloperidol and phenothiazines, which block dopamine receptors, as well as reserpine and tetrabenazine, which deplete biogenic monoamines from their storage sites. In their attempts to produce designer drugs related to meperidine, underground chemists have also synthesized a compound, (MPTP). The toxicity of MPTP is produced by its oxidation to MPP+ (a toxic compound), which selectively destroys the dopaminergic neurons in the substantia nigra.
In some cases, such as in minor leaf veins in the Nicotiana species, virus may load into the CC SE complex directly from BS cells that contact CC and are not separated from them by VP, as in major veins of many plant species (Ding et al. 1995 Santa Cruz et al. 1998). In the case of PVX infection in N. benthamiana, viral CP, which is known to be required for the cell-to-cell movement, is found associated with PD at the BS CC and BS VP interfaces, but not at the VP CC interface (Santa Cruz et al. 1998). This may suggest that the virus preferentially enters the CC directly from the BS cells in minor veins in Nicotiana, bypassing the VP (Santa Cruz et al. 1998). Collectively, these observations suggest that the VP CC boundary (and or BS CC bound
The answer is d. (McPhee, 2 e, pp 155-158 Fauci, 14 e, pp 23482353.) A describes a patient with probable multi-infarct dementia B is a patient with Parkinson's dementia complex or perhaps Lewy body disease C is consistent with the pseudodementia of depression. D is the description most closely associated with Alzheimer's disease although the student should realize that the clinical syndromes may overlap consider
Normal position of the heart, and ventricular hypertrophy can be diagnosed by performing an ECG. Abnormal waves and interval times can point to diseases such as Wolff-Parkinson-White syndrome, an atrioventricular conduction defect, and pericarditis. Detection and monitoring of myocardial infarction is accomplished with the ECG. Figure 14-2 displays the difference between a normal ECG and abnormal recordings as seen in atrial fibrillation, atrial flutter, and tachycardia.
Depression in the elderly is ubiquitous, present in the community, in hospitals, both somatic and psychiatric, in long-stay settings. It can be at the foreground or less evidently present, intermingled with physical diseases or and dementia. Symptoms can be emotional, cognitive and somatic. Emotional disorders include sadness, anxiety, reduction of interest. Sadness is not always evident. It can be minimized or hidden behind an apparently smiling facial expression. A diminished facial mobility, caused by Parkinson's or a multi-infarct cerebral disease, could falsely suggest the presence of sad feelings. Anxiety is often conveyed by somatic complaints, for instance ''pressure'' on the heart or the solar plexus region, an impression of tightening in the throat. Obviously, such symptoms call for investigation for possible physical comorbidities that can coexist with the depressive disorder. A diminished interest is not a symptom restricted to depression and is also a feature observed in...
Treatment and prognosis, of course, are determined by cause(s), and thus an inclusive rather than a reductionistic approach is important. As the severity of dementia progresses over time, the likelihood that more than one cause exists in the same person increases. For example, Lim et a 1 recently reported that only 34 of 94 cases in a community-based Alzheimer's disease (AD) patient registry had pure AD at neuropathology. The remainder frequently had coexisting vascular or Parkinson's disease lesions along with AD.
It is well recognized that the prevalence of depression is considerably increased among people with serious medical problems, such as cancer, Parkinson's disease and stroke 89 . Valvanne et al 90 reported a strong association between major depression and objective ratings of ill-health and functional incapacity in subjects aged 75, 80 and 85 years. In a study of medical inpatients aged over 60 years, the strongest correlate of major depression was severity of medical illness 91 22 and 28 , respectively, of these patients experienced major or minor depression. Minor depression was less strongly correlated with medical illness severity.
Possibly of more concern to the busy clinician are the bio-psycho-social correlates of depression in old age. A strong association exists between physical ill-health and depression, but the patients' view of their own physical health may be adversely affected by their prevailing mood. More objective measures of ill-health, such as cancer, Parkinson's disease and stroke, all produce a consistent excess of depressive illness in sufferers of these conditions. The jury is still out on the association between ill-health and minor depression.
Tacrine to placebo on behavioural items of the ADAS 217 . In a double-blind placebo-controlled trial of metrifonate, a significant superiority of this drug over placebo was found using measures of depression, apathy and hallucinations 218 . The FDA approved cholinesterase inhibitors have all demonstrated effectiveness on behavioural measures for patients with dementia. Donepezil has shown benefit in an open trial of AD patients 219 . Rivas-tigmine has benefitted patients with psychosis associated with Parkinson's disease 220 and DLB 65 . Galanthamine has shown benefit on behavioural measures in AD 221 . Taken together, the effectiveness of the agents on the non-cognitive disturbances associated with dementia probably represents a class effect. Further investigation in this area is necessary to guide prescribing practices.
Although neuroleptic sensitivity and psychosis were proposed as core clinical features in DLB 247 , the attribution of the psychosis should not automatically be made to the disease state. Concurrent medical illnesses and medications commonly cause psychosis. As an example, patients with DLB commonly have parkinsonism and are prescribed antiparkinsonism agents. These medications frequently cause psychosis. Given that neuroleptic sensitivity may be a finding in DLB, atypical antipsychotics should theoretically be useful in treating the psychosis. Initial case reports are disappointing, however, with 3 8 patients with DLB being unable to tolerate even low doses of olanzapine 248 . Our practice is to empirically initiate a gentle titration of an atypical antipsychotic agent for psychosis associated with DLB.
Certain ''core'' similarities of clinical features of depression in younger adults and the elderly have been identified. It is my belief that future research endeavours should focus on those features which are unique to, or at least found predominantly in, the elderly. These include cognitive impairment, neurostructural changes, physical illness both acute and chronic, associated common cerebral organic illnesses such as stroke and Parkinson's disease, and late-onset depression.
Ablation and stimulation techniques and the appearance of pathologies and the results of accidents as well have permitted finding causal relationships among centers and anatomical areas. Certain pathologies demonstrated the existence of feedback loops, as for example in the circuit cerebral cortex-basal ganglia-thalamus-cerebral cortex, which, when malfunctioning, is involved in diseases such as Parkinson's, balism, chorea, and atetosis, all of them collectively named as dyskinesias (from Greek, dys, incorrect, and kinesis, movement). Another CNS feedback circuit is cerebral cortex, which would lead to ataxia or intention tremor. In the Middle Age, some of these diseases were indiscriminately called Saint Vitus' Dance. History in this respect is quite attractive and sometimes sad.
As an active component of the cell death machinery, TG2 is involved in the pathogenesis of several diseases, the enzyme being activated in various disorders 2, 27, 33-35, 55 . TG2 cross-linking activity has been proposed to participate to protein aggregates formation occurring in the major neurodegenerative diseases, including Alzheimer, Parkinson and Huntington's Disease (HD) 56, 57 . In particular, HD is a progressive autosomal-dominant neurodegenerative disorder (incidence 1 in 10,000 individuals), resulting from expanded polyglutamine tracts (beyond 35-40 residues) in the coding region of huntingtin (htt) 58 . The disease is associated with the formation of misfolded ubiquitinated protein aggregates, (neuronal intranuclear inclusions NII), containing all or part of the mutant htt. These protein inclusions have predominantly been detected in the nucleus, but may also be observed in the cytoplasm of striatal and cortical neurons 58 . Several reports suggest that in vitro aggregation...
The caudate nucleus (choice B) is part of the basal ganglia, located immediately lateral to the lateral ventricles. There are at least two important cell types in the caudate. GABAergic projection neurons (the majority) innervate the globus pallidus and substantia nigra pars reticulata. The GABAergic neurons degenerate in Huntington disease, leading to enlarged lateral ventricles that are clearly visible on MRI. The caudate also contains cholinergic interneurons, which provide most of the acetylcholine to the striatum (caudate and putamen). The balance of striatal acetylcholine and dopamine is important for the treatment of patients with extrapyramidal symptoms, such as Parkinson disease or parkinsonism accompanying therapy with antipsychotic medications. The substantia nigra (choice E) is located in the midbrain and consists of the substantia nigra pars compacta and the substantia nigra pars reticulata. The substantia nigra pars com pacta contains the nigrostriatal neurons that are...
The number of hollow-bearing trees on clearfelled sites may be as low as 10-14 of the original number of hollow-bearing trees on that site, and the number of hollow-bearing trees on selectively logged sites seems to be around half of the original number of hollows (Table 4.1), although this will also depend on the number of logging cycles that have occurred at these sites (Chapter 8). For example, in the ash-type forests of the Central Highlands of Victoria, which are clearfelled with limited levels of tree retention, logged sites supported 2-6 hollow-bearing trees per hectare, whereas unlogged sites supported, on average, 14 hollow-bearing trees per hectare (Ambrose 1982). In forests managed under a modified clearfelling regime in East Gippsland and south-eastern NSW, unlogged sites supported, on average, 22 hollow-bearing trees per hectare but comparative logged sites an average of 2-3 per hectare (Gibbons 1999). In north-east NSW, selectively logged moist forests contained around...
In addition to having utility as an antidepressant agent, selegiline has demonstrated the ability to prevent animals from developing a parkinso-nian syndrome induced by 1-methyl-4-phenyl-1, 2, 5, 6-tetrahydropyridine (MPTP). In humans, selegiline dosed at 10mg day may delay the emergence of disability or signs and symptoms of Parkinson's disease.
A 60-year-old man with Parkinson's disease is receiving levodopa cardiodopa therapy and complains of uncontrollable facial movements. Which of the following is correct a. Limb and facial dyskinesias are unusual side effects of chronic levodopa therapy b. Levodopa treatment, while ameliorating symptoms, does not alter the natural history of the disease c. Bromocriptine works by increasing the release of dopamine from the substantia nigra
Drooling requires constant attention from a patient or caregiver, may lead to breakdown of the skin, and is socially disastrous. It is common in cerebral palsy, stroke, and neurodegenerative diseases such as motorneurone disease (ALS) and Parkinsonism (PD). Patients with PD do not produce excessive saliva,15 but do experience reduced swallowing,16 The common forward head posture probably contributes to drooling. Systemic drugs such as anticholinergics may help but are often poorly tolerated, and a few patients undergo surgical denervation or parotid gland irradiation to reduce saliva production. In initial studies with BoNT A in children, in PD and bulbar ALS, up to two thirds of patients reported marked or moderate improvement. However, not all patients experienced relief from their symptoms even when saliva production demon-strably diminished. Clinicians usually injected the parotid glands, and sometimes the submandibular glands. The trials used a variety of injection techniques,...
As you will remember from your study of dysrhythmias, the normal PR interval runs from 0.12 to 0.20s. Shorter intervals indicate accelerated conduction from the atria to the ventricles, such as in Wolf-Parkinson-White (WPW) syndrome or in a junctional pacemaker, which you are already familiar with from your study of dysrhythmias. In WPW syndrome there are congenitally aberrant pathways (Figure 2.3) outside of the normal conduction system that bypass the slowing effect of the AV node and rapidly conduct impulses from the atria directly to the ventricles a kind of electrical short circuit manifested by the classic delta wave (Figure 2.4). Figure 2.4. Wolff-Parkinson-White syndrome as seen in lead II. Note that the ventricles are activated very early, as indicated by the delta wave beginning very shortly after the P wave. Thus, the hallmark of WPW is a delta wave, creating a very short PR interval. Figure 2.4. Wolff-Parkinson-White syndrome as seen in lead II. Note that the ventricles...
A detailed history of known neurological diseases (e.g., stroke, Parkinson's disease, spinal cord injury, multiple sclerosis, myelodysplasia, and so on) is important because these diseases have the potential to affect bladder and sphincteric function. A history of medical diseases such as diabetes or congestive heart failure can cause LUTS by their effects on the lower urinary tract or fluid mobilization.
Recent initiation of symptoms may allow the examiner to determine a transient etiology such as endocrine dysfunction, urinary tract infection, immobility, bowel dysfunction (including fecal impaction), or psychogenic cause. Any of these etiologies, alone or in combination, can produce acute loss of bladder contractile capabilities. Medication dose adjustments or addition of new medications to a therapeutic regimen is a particularly important cause of voiding dysfunction in patients with chronic neurologic conditions such as Parkinson's disease, treatment of which is dependent on several classes of drugs with significant anticholinergic side effects (13).
The head of the caudate nucleus (D) is part of an important element of the motor systems called the basal ganglia. It receives significant inputs from several regions associated with motor functions. These include the cerebral cortex and the dopamine-containing region of the substantia nigra (i.e., the pars compacta). The mediodorsal thalamic nucleus (E) projects large quantities of axons to extensive regions of the rostral half of the frontal lobe, including the prefrontal cortex. It also receives significant projections from the prefrontal region of the cortex.
Food intake and obesity may cause false increases in insulin levels. Recent administration of radioisotopes may affect test results, as will use of oral contraceptives. Other drugs that may cause increased insulin levels include corticosteroids and levodopa.
Improper regulation of cell death is often associated with disease. Decreased apoptosis can result in cancer or auto-immune disorders, while increased or inappropriate apoptosis is a feature of pathologies including AIDS, Alzheimer's disease, and Parkinson's disease (13). It is possible that the inappropriate PCD associated with such diseases may eventually be prevented. However, an understanding of the molecular basis underlying PCD is required before such molecular therapeutics can be developed.
It is worth mentioning the clock face test, in which the patient is asked to draw a clock face and put the hands to indicate a certain time. This is a visuoconstructive test that has been shown to be particularly impaired in dementia with Lewy bodies (DLB), the second commonest cause of degenerative dementia, with or without Alzheimer pathology. In this test, improved performance is not noted in the copy compared to draw part of the test in DLB, in contrast to what is observed in AD, Parkinson's disease and in normal controls 7 . The test may be useful in the clinical setting to differentiate DLB and AD.
Lewy body dementia is a relatively recent addition to the types of dementia, but may be more common than first thought, possibly accounting for 1015 of all dementias. It is characterized by a progressive course. In addition, there is variability in attention and alertness, visual hallucinations and parkinsonism. The diagnostic criteria were first proposed by McKeith et a 24,25 . There maybe falls or transient loss of consciousness, delusions and a sensitivity to neuroleptic drugs. The latter include the newer atypical anti-psychotics. Subsequent work has shown that the diagnostic criteria needed better sensitivity 26 . McKeith et a 27 have now brought out improved criteria, reached by international consensus. A concise overview of the latest information on Lewy body dementia by McKeith et a 28 lays emphasis on the clinical importance of making the diagnosis correctly. This is because it allows identification of patients who are at risk of severe adverse reactions to neuroleptics, but...
The author also reminds us that, despite the identification in recent years of a number of potential biological markers for these disorders, diagnosis still relies primarily on accurate behavioural observation. Much of the work conducted in relation to dementia follows Luria's process-achievement approach, which emphasizes the need for detailed analysis of neuropsycho-logical data to uncover different cognitive processes responsible for patients' overall performance. This approach has also been used to differentiate diseases and clinical syndromes, for example, between frontotem-poral degeneration, Lewy body dementia, Alzheimer's disease (AD) and Parkinson's disease dementia, between AD and cerebrovascular disease, and within some of these forms of dementia, in terms of clinical heterogeneity.
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