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Slowed motor functions characteristic of PD are part of normal aging as well (11 cheap anafranil 25 mg visa depression symptoms anxiety,12) purchase anafranil 25 mg overnight delivery depression with anxiety. Paratonia (gegenhalten) in the elderly who cannot hear properly or are unable to follow instructions due to cognitive impairment may be mistaken as parkinsonian rigidity (8,13,14). Arthritis is common in the elderly, and pain during passive movement at the arthritic joint leads to involuntary resistance resembling rigidity. Flexed posture and impaired postural reflexes, the other major features of PS, are also seen in the normal elderly (10,13,15,16). In general, the age-related abnormalities are symme- trical, while PS is often asymmetrical. Rest tremor, a common early feature of PS (17), is not part of normal aging (18) and hence is the single most reliable feature of this disorder. The most common tremor disorder that is mistaken as PD is essential tremor (ET) (19). Typically, ET is present on positioning a limb against gravity and during activity. ET is usually restricted to the upper limbs and/ or head. By contrast, resting tremor is characteristic of PS/PD and may involve the upper and lower limbs. Nearly one third of these patients develop rest tremor during late stages of the disease (19,20) and, therefore, may be mistaken as PS. For epidemiological surveys, the diagnostic criteria should be simple, consistent through the study interval, and easy to apply. After careful consideration of different diagnostic criteria utilized in epidemiological studies, de Rijk et al. In individuals with preexisting ET, the additional diagnosis of PS should be made only when all three signs are present (19). Parkinson Variants The second major consideration is to classify PS cases into different variants. Most neurologists use the term PD for Lewy body disease (6,7). Distinction between different PS variants is difficult, especially during the early stages of the disease. Even in a clinical setting where patients are repeatedly evaluated by experts, accurate clinical diagnosis may not be possible because the telltale features that distinguish other variants from PD may evolve much later or never (7,21,22). Diagnostic criteria applied retrospectively to autopsied cases (23,24) are not practical in epidemiological studies, which are as a rule based on clinical assessment. Classification into possible, probable, and definite PD (25) has limited value in epidemiological studies, which are primarily aimed at measuring the magnitude of the Copyright 2003 by Marcel Dekker, Inc. Some drug-induced PS patients have underlying idiopathic PD (26), and response to levodopa (LD), though valuable, does not always distinguish between different Parkinson syndromes (27). In one study, when the initial clinical diagnosis of PD was made, only 65% of those cases had PD at autopsy (7). PD is the most common PS variant in clinical (28,29) and pathological series (17). All variants of PS produce significant functional handicap and may improve on the same drugs. Classification into different PS variants is valuable, but it should be recognized that such an exercise would only provide approximate estimates. Autopsy studies to confirm the diagnosis are not possible in epidemiological surveys. Therefore, for descriptive epide- miological studies, all PS variants should be considered. Further classifica- tion may then be made based on the best clinical evidence.

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For instance buy 75 mg anafranil mastercard male depression symptoms uk, in the early stages of PD 50 mg anafranil visa anxiety 20 weeks pregnant, levodopa treatment can improve executive functions normally regulated by the prefrontal cortex. However, this improvement is incomplete and task specific. As the disease advances, patients with a stable clinical response to levodopa fail to exhibit a notable improvement in vigilance and executive function, and patients who exhibit motor fluctuations tend to exhibit transient deterioration in these functions (8). Finally, the effect of these drugs in patients with PD and dementia is likely to be more notable and complex. Other negative iatrogenic influences on cognitive function in PD include the use of drugs like anticholinergics and amantadine, often used to treat tremor and dyskinesias, and psychotropics used to treat sleep disturbances and affective symptoms. These drugs can negatively affect different aspects of memory and attention, particularly in already demented patients. Like these drug effects, many intercurrent medical illnesses and Copyright 2003 by Marcel Dekker, Inc. DEMENTIA: THE PD/AD/LBD OVERLAP SYNDROMES Dementia occurs in approximately 20–30% of PD patients. It represents a major risk factor for the development of many behavioral disturbances, including psychotic symptoms. Dementia appears to be associated with the combined effect of age and the severity of extrapyramidal symptoms (9). Pathologically, up to 40% of autopsy cases with a primary diagnosis of PD have comorbid findings consistent with senile dementia of the Alzheimer’s type (SDAT) (10,11). Conversely, up to 30–40% of patients with SDAT have comorbid parkinsonian features and harbor Lewy body pathology that extends beyond the dopamine neurons in the brainstem to involve the frontal cortex, hippocampus, amygdala, and basal forebrain (12). These defects conspire with aminergic deficits to increase disability and the incidence of psychotropic-induced side effects. They also contribute to the progression of parkinsonian motor symptoms by narrowing the therapeutic window of all antiparkinsonian agents. Lewy body dementia (LBD) is an increasingly recognized syndrome in which dementia is accompanied by spontaneous parkinsonian features, depressive features, and apathy (5,13). Unlike SDAT, this form of dementia exhibits significant fluctuations in arousal ranging from ‘‘narcoleptic-like’’ sleep attacks to delirium in advanced cases. Sleep is often disrupted by sleep fragmentation due to rapid eye movement (REM)–related behavioral disorders. Patients have spontaneous features of PD and are extremely sensitive to drug-induced parkinsonism. Although parkinsonism associated with LBD can be indistinguishable from idiopathic PD, several clinical features tend to help differentiate the two. The course of LBD is more rapid than that of idiopathic PD (5–7 vs. Compared to SDAT patients, LBD patients have spontaneous and drug-induced visual hallucinations early in the course of the illness and frequently exhibit fixed delusions. Although memory is clearly impaired in both conditions, visuospatial and frontal neuropsycho- logical functions are more prominently affected in LBD than in SDAT. BEHAVIORAL AND PSYCHOLOGICAL SYMPTOMS OF DEMENTIA IN PARKINSONIAN SYNDROMES Disturbances of behavior, mood, and perception are common in patients with dementia. These so-called behavioral psychological symptoms of Copyright 2003 by Marcel Dekker, Inc. Clinically they include symptoms prominent in Alzheimer’s disease including apathy, depression, delusional jealousy, paranoia, auditory hallucinations, screaming, and agitation (14). Before DSM-IV helped codify these symptoms as a defined clinical entity, they were thought to be secondary to the distress associated with the dementing process (15). The mechanisms mediating this heterogeneous group of symptoms are poorly understood, but in Alzheimer’s disease and LBD, they appear to be linked to the accumulating cholinergic pathology (16). Clinical and research assessment methods are now being developed to assess these symptoms (17). The aim is to organize the complex array of symptoms of BPSD into logical and empiric clusters that can help guide research and, ultimately, treatment. Several such symptom clusters have been identified: apathy, aggression and agitation, depression, psychosis, and possibly dementia-associated delirium. It should be apparent that these symptoms are not limited to demented patients, nor are they necessarily independent of each other.

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Cells convert the chemical bond energy in foods into other forms buy 50 mg anafranil with mastercard depression symptoms perimenopause, such as an electrochemical gradient across the plasma membrane purchase anafranil 25 mg without prescription anxiety reduction, or the movement of muscle fibers in an arm, or assembly of complex molecules such as DNA (Fig. These energy transformations can be O2 A divided into three principal phases: (1) oxidation of fuels (fat, carbo- hydrate, and protein), (2) conversion of energy from fuel oxidation into the high- energy phosphate bonds of ATP, and (3) utilization of ATP phosphate bond energy to drive energy-requiring processes. O2 CO2 The first two phases of energy transformation are part of cellular respiration, the Cellular overall process of using O and energy derived from oxidizing fuels to generate ATP response 2 ATP. We need to breathe principally because our cells require O2 to generate ade- P i ADP quate amounts of ATP from the oxidation of fuels to CO2. Cellular respiration uses over 90% of the O2 we inhale. Energy transformations in fuel metab- In phase 1 of respiration, energy is conserved from fuel oxidation by enzymes olism. When ATP energy is transformed into that transfer electrons from the fuels to the electron-accepting coenzymes NAD cellular responses, such as muscle contraction, and FAD, which are reduced to NADH and FAD(2H), respectively (Fig. The ATP is cleaved to ADP and Pi (inorganic phos- pathways for the oxidation of most fuels (glucose, fatty acids, ketone bodies, and phate). In cellular respiration, O is used for 2 many amino acids) converge in the generation of the activated 2-carbon acetyl regenerating ATP from oxidation of fuels to group in acetyl CoA. The complete oxidation of the acetyl group to CO2 occurs in CO2. In phase 2 of cellular respiration, the energy derived from fuel oxidation is con- verted to the high-energy phosphate bonds of ATP by the process of oxidative phos- phorylation (see Fig. Electrons are transferred from NADH and FAD(2H) to O2 by the electron transport chain, a series of electron transfer proteins that are located in the inner mitochondrial membrane. Oxidation of NADH and FAD(2H) by O2 generates an electrochemical potential across the inner mitochondrial membrane in the form of a transmembrane proton gradient ( p). This electrochemical potential drives the synthesis of ATP form ADP and Pi by a transmembrane enzyme called ATP synthase (or F0F1ATPase). In phase 3 of cellular respiration, the high-energy phosphate bonds of ATP are used for processes such as muscle contraction (mechanical work), maintaining low intracellular Na concentrations (transport work), synthesis of larger molecules such as DNA in anabolic pathways (biosynthetic work), or detoxification (bio- chemical work). As a consequence of these processes, ATP is either directly or indi- rectly hydrolyzed to ADP and inorganic phosphate (Pi), or to AMP and pyrophos- phate (PPi). The mitochondrial matrix, which is the compartment enclosed by the inner mitochondrial membrance, con- tains almost all of the enzymes for the TCA cycle and oxidation of fatty acids, 337 Fatty acids Glucose Amino acids ATP NADH NADH Pyruvate FAD(2H) Nitrogen NADH Urea Phase 1 of respiration Acetyl CoA The oxidation of fuels Ketone bodies TCA cycle CO2 CO2 FAD(2H) NADH O2 electron transport Phase 2 of respiration H2O chain ATP generation from oxidative phosphorylation ATP + + H+ ADP + Pi + ∆p + Fig. Definitions of prefixes and suffixes ketone bodies, and most amino acids. The inner mitochondrial membrane contains used in describing clinical condi- the protein complexes of the electron transport chain and ATP synthase, the enzyme tions: complex that generates ATP from ADP and Pi. Some of the subunits of these com- an-: Without plexes are encoded by mitochondrial DNA, which resides in the matrix. ATP is gen- -emia: Blood erated in the matrix, but most of the energy-using processes in the cell occur out- hyper-: Excessive, side of the mitochondrion. As a consequence, newly generated ATP must be above normal hypo-: Deficient, continuously transported to the cytosol by protein transporters in the impermeable below normal inner mitochondrial membrane and by diffusion through pores in the more perme- -osis: Abnormal or able outer mitochondrial membrane. Thus, if less energy is required for work, more fuel is stored as glycogen or fat in adipose tissue. The basal metabolic rate (BMR), caloric balance, and G (the change in Gibbs free energy, which is the amount of energy available to do useful work) are quantitative ways of describing energy requirements and the energy that can be derived from fuel oxidation. The various types of enzyme regulation described in Chapter 9 are all used to regulate the rate of oxidation of different fuels to meet energy requirements. After eating, we store excess fatty acids and carbohydrates that are not oxidized as fat (triacylglycerols) in adipose tissue. Between meals, these fatty acids are released and circulate in blood bound to albu- min. In muscle, liver, and other tissues, fatty acids are oxidized to acetyl CoA in the pathway of -oxidation. NADH and FAD(2H) generated from -oxidation are reox- idized by O2 in the electron transport chain, thereby generating ATP (see Fig.

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