Parkinson Disease Medications

The Parkinson's-Reversing Breakthrough

The Parkinson's Breakthrough Program entails the most effective and natural strategies people can use to heal the root cause of Parkinson's Disease. It is a digital manual aimed at showing the users the most effective method for overcoming Parkinson's without high-priced prescription drugs riddled with harmful side effects.The program was not created to be a quick fix. In fact, like different programs, it is tasking. Yet, you will not have to spend a lot of time dealing with it. The system requires your full attention, perseverance, and discipline. For the period of its usage, you will have the opportunity to use to eat some food ingredients that will detoxify you.The methods employed in this book are natural ones that have been proven by many specialists. The users will be privy to what to do and what not to do to treat the underlying root cause of their Parkinson's and the way they can reverse the symptoms naturally and effectively. The system comes with bonus E-books- Lessons from The Miracle Doctors, Mind Control in the USA', and 10 Deadly Health Myths of The 21st Century. The book is in a digital format (PDF) and has been created at a very affordable price. Read more...

The ParkinsonsReversing Breakthrough Summary


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I usually find books written on this category hard to understand and full of jargon. But the writer was capable of presenting advanced techniques in an extremely easy to understand language.

All the modules inside this ebook are very detailed and explanatory, there is nothing as comprehensive as this guide.

Parkinson Diseases Guide By Lianna Marie

Everything About Parkinsons Disease created by Lianna Marie is a new book that covers an effective Parkinsons disease treatment, safe methods, step-by-step techniques, diet plans, natural remedies, and detailed instructions on how to Slow the progression of Parkinsons. Within the All About Parkinsons guide, you will find out the explanation for how Parkinsons disease was born and develop in the very first place. This book is written in pure, easy-to-understand English language that teaches you everything necessary about Parkinsons disease and how to do to prevent as well as treat it forever. Part of the money from every purchase goes to Parkinson's Disease research, to help make a complete cure for this disease possible. Not only will you be getting all the information you need, but your purchase will help prevent others from having to go through the same thing. Read more...

All About Parkinsons Disease Summary

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Author: Lianna Marie
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Association With Parkinsonism And Other Extrapyramidal Disorders

Findings from various centers suggest the following characteristics. First, parkinsonism may be quite prevalent in RBD second, RBD may be the initial manifestation of a parkinsonian disorder in a substantial number of RBD cases initially considered to be idiopathic third, a high percentage of parkinsonian patients without sleep complaints may have either subclinical or clinical RBD fourth, Lewy body pathology may be quite prevalent in RBD and fifth, similar findings have been reported in various extra-pyramidal disorders. A review of the world literature on RBD identified 280 published cases, of which 149 (53 ) were closely associated with a neurological disorder (Schenck and Mahowald, 1996a). A parkinsonian disorder was the most prevalent neurological condition, affecting 43 (n 64) of neurologically disordered RBD patients (representing 23 of n 280 total cases) narcolepsy was the next most prevalent condition, affecting 25 (n 38) of neurologically disordered RBD patients...


The delayed emergence of a parkinsonian disorder in RBD has been reported in a group of 29 male patients 50 years of age who were initially diagnosed to have idiopathic RBD (Schenck and Mahowald, 1996c). Of these, 38 ( ) eventually developed a parkinsonian disorder presumably Parkinson's disease (PD) at a mean interval of 3.7 1.4 years after the diagnosis of RBD, and at a mean interval of 12.7 7.3 years after the onset of RBD. Only 7 ( J of those patients had, at the time of publication, developed any other neurological disorder. RBD was controlled with nightly clonazepam treatment in 89 (f ) of patients (both groups). Thus, RBD can be the heralding manifestation of PD (by many years) in a substantial subgroup of older male RBD patients. However, a number of presumed PD patients could eventually be diagnosed with multiple system atrophy (striatoni-gral degeneration subtype). The findings from that report indicate the importance of serial neurological evaluations after the initial...

Spread of Metabolic Activation during Seizures

In young rats until the third week of age, kai-nic acid-induced status epilepticus produces a rise in metabolism restricted to the hippocampus and lateral septum (28, 130). This is paralleled by paroxysmal discharges observed on electroencephalogram (EEG) that are recorded in the hippocampus, although some studies have proposed that seizures are more prominent in the neocortex (28, 130, 132, 140, 141). Starting from the end of the third week, there is a rise in labeling of other structures that are part of or closely associated with the limbic system the amygdala complex, the mediodorsal and adjacent thalamic nuclei, the piriform, entorhinal, and rostral limbic cortical regions, and areas of projection of the fornix. These metabolic maps are thus similar to those observed in adults (130, 142). In amygdala kindling in PN15, the metabolic activation during severe seizures is restricted to limbic structures (128, 129), even when the rats experience secondarily generalized seizures....

Brain Structures Controlling Seizures

Two compartments of the substantia nigra pars reticulata (SNR) that in the adult rat brain differentially control seizures. Sagittal section of the rat brain 2.4 mm lateral from midline (168) limited to parts of diencephalon, midbrain, and the brainstem. The diagram illustrates both subregions of the SNR. In the adult male brain, microinfusions of muscimol placed bilaterally and symmetrically in the light gray area (SNRanterior) have anticonvulsant effects in flurothyl-induced clonic seizures. In the adult male brain, bilaterally symmetrical microinfusions of muscimol in the dark gray area (SNRposterior) have proconvulsant effects. In the adult female brain, symmetrical microinfusions of muscimol into SNRanterior have similar anticonvulsant effects as in the adult males. However, symmetrical muscimol infusions into SNRposterior in adult female rats are without any effect on seizures. Arrows mark the main directions.

Limitations In The Biological Realism Of Current Neural Network Models

Network models that include more detailed 3D information would have a number of advantages. A more thorough validation of the model connectivity would be possible through direct comparison with detailed anatomical measurements, which are available for several brain regions including cortex (Somogyi et al., 1998 Thomson et al., 2002 Douglas and Martin, 2004) and cerebellum (Harvey and Napper, 1991 Sultan and Bower, 1998). This is particularly important for brain regions with complex synaptic connectivity patterns such as the cortex. Associating cells and synapses in the model with specific 3D locations could also be used to simulate other important aspects of brain function including the diffusion of signaling molecules and metabolites. The rate at which a diffusant decays (and the peak concentration reached at a particular distance) from an instantaneous point source depends strongly on the number of spatial dimensions, with 3D geometries decaying most rapidly (Crank, 1993)....

Mitochondrial cytopathy myoclonic epilepsy with ragged red fibres [MERRF

The clinical features are variable, even within families. The EEG shows spike-wave at 2-5 Hz with a slow background. Ragged red fibres are found on muscle biopsy in 80 of cases, and biochemical analysis will show decreased activity in respiratory chain enzymes. MRI may show atrophy, T2 signal change and also basal ganglia calcification. In 90 of cases the genetic defect is an A-to-G transition at nucleotide-8344 in the tRNAlys gene of mtDNA, and some other cases are caused by T8356C or G8363A mutations. Genetic testing is available. Heteroplasmy is responsible for some of the phenotypic variation and can complicate genetic diagnosis.

Electrical Brain Stimulation

Following the success of treatment for movement disorders, deep brain stimulation (DBS) is under active investigation as a non-pharmacological therapeutic modality for patients with medically intractable epilepsy who are not eligible for resective surgical procedures 66 . A variety of anatomical structures may be targeted, including deep brain structures 67, 68 . Interest in the stimulation of subcortical structures stems from the recognition of widespread non-specific anterior and intralaminar nuclear connections to many other parts of brain and the progressive recruitment of substantia nigra, subthalamic nucleus and midline thalamic nuclei in animal models of epilepsy 66 . Furthermore, automated seizure detection can be incorporated into an electrical brain stimulator to form a closed-loop system so that electrical stimulation is delivered to the epileptogenic zone when onset of ictal activity is detected 69, 70 . Recent understanding in seizure dynamics also helps decipher the...

Method of controlling epilepsy by brain stimulation

Abstract A method of preventing seizures as experienced by persons with Epilepsy. High frequency electrical stimulation pulses are supplied to the subthalamic nucleus thereby blocking neural activity in the subthalamic nucleus and reducing excitatory input to the substantia nigra which leads to a reduction in the occurrence of seizures.

Diagnostic approach

Based on the clinical presentation and progression of cognitive loss, associated symptoms, and ethnic origin, most of the other progressive myoclonic epilepsies can be potentially diagnosed. Other than the canonical features of myoclonus, generalized seizures, ataxia, and ragged red fibers in muscle, there are frequent other clinical abnormalities noted in MERRF, including sensorineural hearing loss, peripheral neuropathy, short stature, exercise intolerance, and optic atrophy. Less frequent clinical signs reported are cardiomyopathy, preexcitation arrhythmia (Wolf-Parkinson-White), pigmentary retinopathy, ophthalmoparesis, pyramidal signs, and multiple lipomas

Effects Of Drugs On Serum Prolactin Levels

The effects of the newer atypical antipsychotic drugs on serum PRL have been inconsistently reported. A relatively high affinity for the 5-HT2 serotonergic receptor and relatively low affinity for the D-2 dopa-mine receptor differentiates these drugs from the phe-nothiazines, which are prone to produce high elevations of serum PRL and more likely to cause parkinsonism. Most studies show modest elevations of serum PRL with risperidone but no significant effects from clozap-ine or olanzapine (4-6).

Changes In Serum Prolactin Levels With Pathologic States

Skin lesions of thoracic dermatomes Pituitary prolactinomas Hypothalamic lesions Parkinson's disease Epileptic seizures Medical treatments General anesthesia Surgery Drugs Dopamine antagonists Atypical antipsychotics Phenothiazines Methyldopa Haloperidol Reserpine Serotonergic drugs Antiepileptic drugs Carbamazepine Phenytoin Estrogen serum PRL. Pituitary tumors, such as PRL-secreting microadenomas (prolactinomas), produce sustained elevations of serum PRL. Skin lesions that affect mid-thoracic dermatomes at the level of the breasts or radicular lesions at that level may cause sustained hyperpro-lactinemia. Patients with Parkinson's disease sometimes experience moderate hyperprolactinemia because of the diminished dopaminergic inhibition of PRL secretion. Physical stressors, such as surgery or anesthesia, produce a transient elevation of serum PRL.

Inhalation Of Convulsant Substances

The pattern of metabolic involvement depends on the seizure type and whether in ictal or postictal state (Veliskova et al., 2005, in press). In immature rats, mild seizures induce decreases in 2DG uptake while severe seizures produce increases in the brain-stem and decreases in the cortex (Szot et al., 2001). In adult rats, c-fos immunoreactivity after flurothyl seizures was found throughout the cortex PN10 rats had immuno-positivity only in the deep neocortical layers (Jensen et al., 1993). This approach is frequently used to create an acute or chronic seizure focus in a particular brain area, usually in the cortex. Additional structures may be injected with a con-vulsant substance, such as the hippocampus, amygdala, substantia nigra, area tempestas, etc. Many of the convulsant drugs can be injected in a solution into the brain ventricular system. Some of these ICV administrations have already been mentioned herein. The advantage of this approach is that...

Neurotoxic sideeffects

The sedative side-effects typical of antiepileptic drugs also occur with valproate, severely so in about 2 of patients, and sometimes associated with other neurological symptoms such as confusion and irritability. Tremor occurs in about 10 of patients on valproate, and is dose-related but usually mild. Parkinsonism seems to be another uncommon but unusual side-effect of vaproate therapy, usually developing on long-term treatment and reversible on drug withdrawal. The mechanism is unclear.

Treatment and outcome

As the valproate dose was reduced, her physical and cognitive condition improved significantly. Valproate was then completely withdrawn, resulting in complete remission of both the cognitive impairment and the parkinsonian syndrome. Subsequently, the EEG showed normalization of the background activity and resolution of the generalized epileptiform activity. In addition, this case shows that treatment with valproate may cause a syndrome that imitates Parkinson's disease. The insidious onset of valproate-associated movement disorder - after months or years of otherwise well-tolerated treatment with valproate - increases the probability that these symptoms may be mistaken for a neurodegenerative disease.1,2,5 In this case, clinical symptoms, hyperammonemia and EEG findings led to the diagnosis of valproate-induced encephalopathy. It should be noted that the serum valproate concentration was only moderately elevated above the therapeutic range. This observation is consistent with several...

Entitled to Respect A National Survey of Teens Attitudes and Behaviors About Epilepsy and Acceptance Executive Summary

Summary Entitled to Respect A National Survey of Teens' Attitudes and Behaviors About Epilepsy and Acceptance Executive Summary summarizes the results of a survey of teens' attitudes and behaviors about epilepsy. The survey consisted of a questionnaire that was distributed to teens throughout the United States by 20 affiliates of the Epilepsy Foundation from March through July 2001 in schools selected by the affiliates. The questionnaire asked about respondents' (1) demographics (2) awareness of epilepsy (3) knowledge of epilepsy (4) perceived stigmas associated with epilepsy and (5) awareness of muscular dystrophy, human immunodeficiency virus infection acquired immunodeficiency syndrome, arthritis, diabetes, breast cancer, and Parkinson's Disease. Results are based on 19,441 usable questionnaires. Thirty-six percent of the respondents felt that kids with epilepsy are likely to get picked on or bullied more than other kids. Only 25 percent felt this is unlikely to happen. Thirty-one...

Brain Mechanisms in Combined RBDExtrapyramidal Disorders

What brain mechanisms may be involved in subclinical and clinical RBD associated with various extrapyramidal disorders The pedunculopontine nucleus (PPN) is likely to be prominently involved in the disruption of the REM-atonia circuitry, for at least three reasons. First, there is a strong reciprocal connectivity between the PPN and the substantia nigra (Garcia-Rill, 1991), the main site of pathology accounting for the cardinal signs of PD (Koller, 1992). Second, the neuropathology of PD includes prominent neuronal loss within the PPN (Jellinger, 1992). The retrorubral nucleus is located near the substantia nigra, and appears to be implicated in the linked PD-RBD pathology (Lai and Siegel, 1990). The retrorubral nucleus projects to the caudate and putamen (extrapyramidal motor system) experimental lesions to the retrorubral nucleus in cats releases abnormal motor activity during both sleep and wakefulness, ranging from myoclonic twitches to rhythmic leg movements and locomotion (Lai...

Pharmacotherapy Of Anxiety Disorders In

As shown in Table 15.2, several of the SSRIs have shown efficacy in GAD and PD all SSRIs have also shown efficacy in OCD, but in contrast to the treatment of GAD and PD, a therapeutic effect may not be noticed for 6-12 weeks. However, a cautionary note is in order patients with PD may be extremely sensitive to adverse events of psychotropic drugs. Accordingly, a lower initial dose should be considered and a slower titration followed than those in the treatment of mood disorders. In the case of GAD and PD, absence of desired therapeutic effect with an SSRI should be followed by a trial with the SNRI venlafaxine or duloxetine. As in the case of mood disorders, the anxiolytic effect of these drugs may not be Among the older anti-depressant drugs, the TCA imipramine is the agent of choice in PD with a comparable efficacy to that of SSRIs and has also been found to be as effective as benzodiazepines in the treatment of GAD. MAOIs are also effective in the treatment of PD. In addition to...

Lglutamate Signal Analysis

Comparison of release and uptake parameters in our laboratory has allowed us to characterize glutamate regulation in normal and aged animals and also to explore the role of glutamate in Parkinson's disease, amyotrophic lateral sclerosis and attention-deficit hyperactivity disorder through animal models. As stated earlier, our glutamate-sensitive MEA can be utilized not only for real-time monitoring of resting glutamate levels, but also for investigation of complex release and or uptake mechanisms. A better understanding of the glutamate neurotransmission dysregulation present in epilepsy may offer novel therapeutic targets and diagnostic techniques, in addition to more accurate seizure prediction. Glutamate regulation characteristics may also become important in rapidly distinguishing diseased from non-disease tissue. This could prove very helpful to neurosurgeons performing seizure focus resection surgery.

Other Functional Surgical Procedures

There has been a recent resurgence of interest in deep brain stimulation (DBS), encouraged by both the improved anatomical precision of stereotaxy made possible by MRI, better surgical instrumentation and stimulation technology, and also by the success of these procedures in other conditions such as Parkinson disease and in pain. Targets that are most favoured include the caudate nucleus, the centro-median nucleus of the thalamus, the anterior thalamic nucleus, the mamillary bodies and the subthalamic nucleus. Direct stimulation of the epileptic focus, in both the neo-cortex and the hippocampus, has also been attempted. All these approaches have had encouraging results in animal experimentation, and there are small human case reports and small series. Pioneering double-blind studies in small numbers of patients with severe epilepsy have been reported. In six of nine patients, stimulation of the subthalamic nuclear resulted in an > 80 reduction in seizures, and in a study of five...

Paroxysmal Dyskinesia

At this time, antiepileptic agents remain the standard form of treatment for patients with paroxysmal dyskinesia (45). Other medications that have been tried include levodopa, tetrabenazine, and trihexyphenidyl. There is some evidence that patients with PKD respond better to antiepileptic medications than patients with PNKD.

Association Of Rapid Eye Movement Sleep Behavior Disorder With Specific Human Leukocyte Antigen Haplotypes

Arnulf, I., Bonnet, A.-M., Damier, P., Bejjani, B.-P., Seilhean, D., Derenne, J.-P., and Agid, Y. (2000). Hallucinations, REM sleep, and Parkinson's disease a medical hypothesis. Neurology 55 281-288. Boeve, B. F Silber, M. H Petersen, R. C., Kokmen, E., Parisi, J. E., and Olson, E. J. (1997). REM sleep behavior disorder and degenerative dementia with or without parkinsonism A syndrome predictive of Lewy body disease Neurology 48 A358-A359. Cornelia, C. L., Tanner, C. M., and Ristanovic, R. K. (1993). Polysomnographic sleep measures in Parkinson's disease patients with treatment-induced hallucinations. Ann. Neurol. 34 710-714. Datta, S., Dossi, R. C., Pare, D., Oakson, G., and Steriade, M. (1991). Substantia nigra reticulata neurons during sleep-waking states Relation with ponto-geniculo-occipital waves. Brain Res. 566 344-347. Eisensehr, I., Linke, R., Noachtar, S., Schwarz, J., Gildehaus, F. J., and Tatsch, K. (2000). Reduced striatal dopamine transporters in idiopathic rapid eye...

Temporal Gate hypothesis

In other neurological conditions associated with deterioration, the phenomenon of oxidative stress (the production of oxygen radicals beyond a threshold for proper antioxidant neutralization) has been implicated. These include Alzheimer's disease (Sims, 1996), Parkinson's disease (Jenner and Olanow, 1994), amyotrophic lateral sclerosis (Gorman et al., 1994), Pick's disease (Castellani et al., 1995J and schizophrenia (Ramchand et al., 1996). Various intracellular messenger systems involving glutamate are implicated in oxidative radical production. These systems are involved in neuronal growth, differentiation and apoptosis (Michaelis, 1998). Glutamate is also known to play an important role in epilepsy. The author has observed substantial improvement in cognitive functioning in two patients (one male 'subcortical', one female 'temporal') after using lamotrigine, a glutamate release inhibitor (Meldrum, 1994). There are various other reports, generally of an anecdotal nature, of the...

Rem Behavior Disorder

RBD has been associated with brainstem lesions caused by vascular disease, trauma, and multiple sclerosis (59). In addition, RBD is common in patients with Parkinson's disease (60-62), and it has been reported in patients with narcolepsy (63). Schenk et al. followed patients who were diagnosed with RBD and found that 38 developed Parkinson's disease at an interval of 3.7 1.4 years (60). Treatment for RBD with clonazepam (0-5-2.0 mg.h.s) is successful in 80 to 90 of patients (59). Clonazepam does not completely suppress the motor activity during REM sleep, but it usually eliminates the vigorous, coordinated movements characteristic of RBD episodes. This allows the patient to sleep without disruption. If clonazepam is unsuccessful or causes drowsiness, tricyclics, levodopa carbidopa, clonidine, or carbamazepine may be tried. Donepezil, an acetyl-cholinecterase inhibitor, has been effective in some patients (64). 57. Kaplan PW, Allen RP, Buchholz DW, Walters JK. A double-blind,...

The biological significance of phenomenological similarities between PD and epilepsy

Integrating the previous models into a theory, Windmann (1998) proposes what he calls the 'false-alarm-theory of PD'. Symptoms of panic and pathological states of anxiety arise from the hyperfunctioning of a preattentive alarm system whose structural basis is closely related to the amygdala and its connections to ascending neuromodulatory transmitter systems. The hyperfunction results in a tendency to signal potential threat to the neocortex which is not adequately modified by more elaborated processing in patients with PD.

Biochemical pathophysiology

As yet, no specific defect in GABA functioning has been identified in patients with PD. However, GABA is indirectly implicated in PD through benzodiazepines. Benzodiazepine receptor agonists produce neuronal inhibition via benzodiazepine receptor modulation of GABAa receptor mechanisms, leading to, amongst other effects, anxiolysis, muscle relaxation and sedation. Benzodiazepine antagonists occupy the benzodiazepine receptor site without producing pharmacological effects, while inverse agonists, such as beta-carboline, are anxiogenic and procon-vulsant (Katz et al., 1993). Clinical data show that high potency benzodiazepine agonists, such as alprazolam and clonazepam, have marked antipanic effects. Moreover, other studies have suggested subsensitivity of benzodiazepine receptors in these patients (Eison, 1990). Possibly in relation to this, flumazenil, a benzodi-azepine antagonist, has been reported to be panicogenic in patients with PD but not in healthy controls.

Pharmacomechanistic Approach to AED Combinations

Combining drugs with different mechanisms of action is a common strategy in the treatment of many medical disorders. Polytherapy is also used routinely in some neurological conditions, even at treatment initiation. Thus, in patients with Parkinson's disease, levodopa is combined with a dopa decarboxylase or catechol-o-methyltransferase inhibitor to reduce

Druginduced seizures

Theophylline is a potent convulsant which can result in seizures or status epilepticus, possibly due to the anti-adenosine action. P-blockers and other antiarrhythmic agents have been reported to precipitate seizures, particularly in overdose. Cimetidine, levodopa, insulin, thiazide diuretics, lidocaine, salicylates, chemotherapeutic agents, L-asparaginase and baclofen have been reported to cause seizures. The non-steroidal analgesics also predispose to seizures (for example NSAIDs, tramadol, diamorphine and pethidine).

REM Sleep Disorders

Behavioral management and treatment of any comorbid medical conditions are the appropriate treatment strategies. The onset of a REM behavior disorder may rarely be the first clinical sign of a brainstem lesion, and neuroimaging may be appropriate. In adults REM behavior disorders and acting out of dreams, sometimes violent, may predate by many years other symptoms of serious neurological disorders such as Parkinsons disease, dementia with Lewy bodies, or multiple system atrophy.51

Other Issues

Tremor and or parkinsonian symptoms can be seen with valproic acid use. Lastly, hyponatraemia occurs with either carbamazepine or oxcarbazepine. Therefore, patients who are sodium depleted, have fluid electrolyte abnormalities or are receiving diuretics should be careful when utilizing these agents. The elderly are at increased risk of hyponatraemia with these agents (up to 6-7 ), and their electrolytes should be monitored on a routine basis.

Biological Basis

Emotional stress is the most commonly reported precipitant of bruxism (Rugh and Harlan, 1988b). Medications including amphetamines (Ashcrost et al., 1965) and levodopa (L-dopa) (Magee, 1970) may precipitate this disorder long-term phenothiazine use (Kamen, 1975) and alcohol (Hartmann, 1979) have also been related to bruxism. Bruxism may have a genetic predisposition. Although bruxism has been postulated to be a centrally mediated sleep disorder on the basis of these observations, the specific mechanisms underlying this disorder are poorly understood.


It is generally accepted that alterations in central dopamine levels are responsible, in part, for the onset and continuance of many seizure disorders (see 174 for a review). In the midbrain, inhibition of the substantia nigra (SN) has been shown to attenuate seizures in many animal models of seizure disorders. The SN projects dopaminergic neurones to the caudate putamen and, in turn, receives GABAergic afferents from the caudate putamen via one of two pathways. The first pathway, commonly known as the direct pathway, offers a direct monosynaptic GABAergic projection from the caudate putamen to the SN. The second pathway (indirect pathway) involves a GABAergic projection from the caudate putamen to the lateral globus pallidus. The globus pallidus then projects GABAergic efferents to the subthalamic nucleus that finally exerts glutamatergic tone onto the SN.

The limbic system

Ventral Hippocampus

The hippocampus also receives direct cholinergic and GABAergic input from the septal area, which mediates the classical hippocampal theta rhythm, and these projections may have disinhibitory as well as inhibitory influences on epileptic activity. With respect to brain stem afferents, direct noradrenergic input to the hippocampus from the locus coeruleus can be excitatory (Madison and Nicoll, 1986), while serotonergic input from the raphe nucleus and dopaminergic input from the substantia nigra and ventral tegmental area are predominantly inhibitory (Andrade and Nicoll, 1987), but biogenic amine effects can be varied, depending on the postsynaptic target. Indirect afferent influences on the hippocampus, via entorhinal cortex, derive from a large area of neocortex, including frontal limbic regions responsible for goal-directed behaviour, cingulate cortex influencing memory, all sensory cortical areas for integration of polymodal sensory information, and perirhinal and piriform cortex,...


A variety of abnormal electrophysiological findings have been reported in groups of patients with PD in comparison with healthy control subjects. However, other studies have failed to detect any EEG changes resembling epileptiform activity in people with PD. Stein and Uhde (1989) evaluated a group of 35 medication-free patients with PD (Research Diagnostic Criteria). The EEGs were performed over 45 to 75 minutes by using a 21-channel scalp EEG. In addition, 31 patients had an EEG performed with additional use of nasopharyngeal or anterior temporal leads. Twenty-two patients had been sleep-deprived for 24 hours before the EEG, and recordings were performed during drowsiness or light sleep whenever possible. In all patients, EEGs were obtained during a 2-minute period of hyperventilation and in response to photic stimulation. Patients were divided into two groups 15 with psychosensory symptoms and 20 without psychosensory symptoms. In agreement with Stein and Uhde's work, Lepola et al....

Scott C Baraban

Pediatric epilepsy models are confined primarily to rodents. Although using a rodent model of a human neurologic disorder has distinct advantages, there is no rationale to support our almost exclusive reliance on this species. Indeed research questions related to genetic modifiers of pediatric epilepsy syndromes, high-throughput anticonvul-sant drug screening, and rapid genetic manipulations aimed at analysis of basic cellular mechanisms of epilepto-genesis could be better suited to a simple vertebrate system. Exciting new discoveries in the general field of neurobiol-ogy exploit the experimental advantages of simpler organisms such as Caenorhabditis elegans (worms), Drosophila melanogaster (fruit flies), and Danio rerio (zebrafish). Analysis of Parkinson (parkin) gene function in flies (Pesah et al., 2004) and discovery of daf genes regulating the aging process in worms (Hsin and Kenyon, 1999 Lin et al., 1997) are just two examples. Similar discoveries are possible in the epilepsy...

Panic disorder

The clinical diagnosis of PD is characterized by panic attacks, avoidance of situations in which previous panic attacks have occurred and ongoing worry regarding the possibility of future attacks. However, these recurrent attacks of extreme fear and a feeling of impending death or disaster are not restricted to any particular environmental setting or set of circumstances. In addition, it is important to note that although patients with PD worry about having further panic attacks, this worry is of a lower magnitude than the emotions experienced during an attack. There is good evidence, based on clinical accounts, that PD is not a homogeneous disorder. In some people pure PD exists with panic attacks in the absence of any other psychopathology. However, sizeable proportions of those with PD are comor-bid for agoraphobia or depression or both. It has been reported that women with PD are more likely to report depression, anxiety or agoraphobic avoidance than men with this diagnosis...


Whereas neurocardiogenic syncope is fairly benign, cardiac syncope is potentially fatal. Causes include either cardiac arrhythmias (e.g., Wolff-Parkinson-White syndrome, long QT syndromes) or structural heart disease (e.g., hypertrophic cardiomyopathy, aortic stenosis). These require an accurate history, a full neurological and cardiac examination, ECG, echocardiography, and even prolonged ECG monitoring (24-hour or embedded long-term monitoring).

Lewy Body Disease

Lewy body disease, as a postmortem finding, was reported in an 84-year-old man with a 20-year history of RBD, but without any clinically detected neurological disorder (Uchiyama et al., 1995). Postmortem histopathological examination revealed that the patient had Lewy body disease with marked decrease of pigmented neurons in the locus ceruleus and substantia nigra. These findings represent the first documented evidence of a loss of brain stem monoaminergic neurons in clinically idiopathic RBD, and suggest that Lewy body disease might provide an explanation for idiopathic RBD in elderly patients. This report is important in that it calls attention to the possibility that a sizable subgroup of RBD patients with presumed idiopathic RBD may, in fact, turn out to have Lewy body disease as the neuropathological basis of RBD. A subsequent report involved the case of a 73-year-old man with a 2-year history of parkinsonism and a 15-year history of RBD (Negro and Faber, 1996). The clinical...

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