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Many anticonvulsant oral medications are available for the management of temporal lobe seizures. Most anticonvulsants function by decreasing the excitation of neurons, for example, by blocking fast or slow sodium channels or by modulating calcium channels; or by enhancing the inhibition of neurons, for example by potentiating the effects of inhibitory neurotransmitters like GABA.
In TLE, the most commonly used older medications are phenytoin, carbamazepine, primidone, valproate, and phenobarbital. Newer drugs, such as gabapentin, topiramate, levetiracetam, lamotrigine, pregabalin, tiagabine, lacosamide, and zonisamide promise similar effectiveness, with possibly fewer side-effects. Felbamate and vigabatrin are newer, but can have serious adverse effects so they are not considered as first-line treatments.
Up to one third of patients with medial temporal lobe epilepsy will not have adequate seizure control with medication alone. For patients with medial TLE whose seizures remain uncontrolled after trials of several types of anticonvulsants (that is, the epilepsy is "intractable"), surgical excision of the affected temporal lobe may be considered.
The use of a regimented diet is an approach that has been found to help control seizures in children with severe, medically intractable frontal lobe epilepsy. Although the use of dieting to prevent seizures from occurring is a lost treatment that has been replaced by the use of new types of anticonvulsants, it is still recommended to patients to this day. A ketogenic diet is a high-fat, low-carbohydrate based diet that patients are typically asked to follow in conjunction with their anticonvulsant medications. This diet was designed in order to mimic many of the effects that starvation has on the metabolic functioning of the body. By limiting the amount of carbohydrates and increasing the amount of exogenous fats available to the metabolism, the body will create an excess of water-soluble compounds known as ketone bodies. Although the mechanism of action is still unknown, it is believed that these excessive amounts of ketone bodies become the brain's main source of energy and in turn are able to suppress the frequency of seizure occurrence.
There are several different ways to treat frontal lobe epileptic seizures, however, the most common form of treatment is through the use of anticonvulsant medications that help to prevent seizures from occurring. In some cases, however, when medications are ineffective, a neurologist may choose to operate on the patient in order to remove the focal area of the brain in which the seizures are occurring. Other treatments that can be administered to aid in reducing the occurrence of seizures include the implementation of a specific, regimented diet and/or the implantation of a vagus nerve stimulator.
Epilepsy surgery has been performed since the 1860s and doctors have observed that it is highly effective in producing freedom from seizures. However, it was not until 2001 that a scientifically sound study was carried out to examine the effectiveness of temporal lobectomy.
Temporal lobe surgery can be complicated by decreased cognitive function. However, after temporal lobectomy, memory function is supported by the opposite temporal lobe; and recruitment of the frontal lobe. Cognitive rehabilitation may also help.
Unfortunately, there is no real way to prevent against vertiginous episodes out of the means of managing the disease. As head trauma is a major cause for vertiginous epilepsy, protecting the head from injury is an easy way to avoid possible onset of these seizures. With recent advances in science it is also possible for an individual to receive genetic screening, but this only tells if the subject is predisposed to developing the condition and will not aid in preventing the disease.
There is a range of ways to manage vertiginous epilepsy depending on the severity of the seizures. For simple partial seizures medical treatment is not always necessary. To the comfort of the patient, someone ailed with this disease may be able to lead a relatively normal life with vertiginous seizures. If, however, the seizures become too much to handle, antiepileptic medication can be administered as the first line of treatment. There are several different types of medication on the market to deter epileptic episodes but there is no support to show that one medication is more effective than another. In fact, research has shown that simple partial seizures do not usually respond well to medication, leaving the patient to self-manage their symptoms. A third option for treatment, used only in extreme cases when seizure symptoms disrupt daily life, is surgery wherein the surgeon will remove the epileptic region.
There have been early and consistent strategies for measurement to better understand vertiginous epilepsy including caloric reflex test, posture and gait, or rotational experimentation.
In Japan, Kaga et al prepared a longitudinal study of rotation tests comparing congenital deafness and children with delayed acquisition of motor system skills. They were able to demonstrate the development of post-rotation nystagmus response from the frequency of beat and duration period from birth to six years to compare to adult values. Overall, the study demonstrated that some infants from the deaf population had impaired vestibular responses related to head control and walking age. A side interpretation included the evaluation of the vestibular system in reference to matching data with age.
Research in this area of medicine is limited due to its lacking need for urgent attention. But, the American Hearing Research Foundation (AHRF) conducts studies in which they hope to make new discoveries to help advance treatment of the disease and possibly one day prevent vertiginous seizures altogether.
Treatment for topographical disorientation has been achieved through a case by case basis. Prognosis is largely dependent on the organic cause. Neuropsychological assessment followed by an assessment of unaffected cognitive abilities can be employed in therapy. Treatment for recovering navigational skills require strengthening unaffected navigational strategies to bypass defective ones.
Deep brain stimulation of the anterior nuclei of the thalamus is approved for DRE in some countries in Europe, but has been and continues to only be used in a very few patients. After 5 years of DBS a seizure reduction of 69% and a 50%-responder rate of 68% was reported in a randomized-double blinded trial. The rate of serious device related events was 34% in this study.
Responsive neurostimulation (RNS) is approved for DRE in the USA and involves stimulation directly to 1 or 2 seizure foci when abnormal electrocorticographic activity is detected by the devices software. After 2 years of RNS a seizure reduction of 53% was reported in a randomized-double blinded trial as well as a rate of serious device related events of 2.5%.
Transcutaneous vagus nerve stimulation (tVNS) is approved for DRE in some European countries and involves externally stimulating the auricular branch of the vagus nerve in the ear. tVNS failed to demonstrate efficacy in a first randomized-double blinded trial: responder rates did not differ between active and control groups potentially indicating a placebo effect behind the 34% seizure reduction seen in the patients who completed the full follow-up period.
A modified Atkins diet describes the long term practice of the first phase of the popular Atkins diet the so-called induction phase to reduce seizures through ketosis. In this diet the fat content of the nutrition is slightly lower than in the ketogenic diet at around 60%, the protein content is around 30% and the carbohydrate content is around 10% rendering the diet less restrictive and more compatible with the daily life compared to the ketogenic diet. Several studies show that the modified Atkins diet produces a similar or slightly lower seizure reduction to the ketogenic diet. Some physicians, especially in the USA, recommend the modified Atkins diet because they assume that patients will adhere to it on the long-term because it is more compatible with daily life and the meals are more enjoyable. It has also been concluded in another study that the diet is well tolerated and effective in hard to treat childhood epilepsy.
In adults, many of the symptoms diminish over time. Although it has been suggested that a similar diminishing of symptoms occurs in children as well, it appears more likely that most do not overcome their deficits, but instead simply learn to adjust.
Serotonin and norepinephrine reuptake inhibitor, venlafaxine, were given to case study KS four months after initial stroke that started symptoms of witzelsucht. Changes back to his original behavior were noticeable after daily dose of 37.5 mg of venlafaxine for two weeks. In subsequent two months, inappropriate jokes and hypersexual behavior were rarely noticed. Due to the rareness of this disorder, not much research into potential treatments has been conducted.
In regard to anosognosia for neurological patients, no long-term treatments exist. As with unilateral neglect, caloric reflex testing (squirting ice cold water into the left ear) is known to temporarily ameliorate unawareness of impairment. It is not entirely clear how this works, although it is thought that the unconscious shift of attention or focus caused by the intense stimulation of the vestibular system temporarily influences awareness. Most cases of anosognosia appear to simply disappear over time, while other cases can last indefinitely. Normally, long-term cases are treated with cognitive therapy to train patients to adjust for their inoperable limbs (though it is believed that these patients still are not "aware" of their disability). Another commonly used method is the use of feedback – comparing clients' self-predicted performance with their actual performance on a task in an attempt to improve insight.
Neurorehabilitation is difficult because, as anosognosia impairs the patient's desire to seek medical aid, it may also impair their ability to seek rehabilitation. A lack of awareness of the deficit makes cooperative, mindful work with a therapist difficult. In the acute phase, very little can be done to improve their awareness, but during this time, it is important for the therapist to build a therapeutic alliance with patients by entering their phenomenological field and reducing their frustration and confusion. Since severity changes over time, no single method of treatment or rehabilitation has emerged or will likely emerge.
In regard to psychiatric patients, empirical studies verify that, for individuals with severe mental illnesses, lack of awareness of illness is significantly associated with both medication non-compliance and re-hospitalization. Fifteen percent of individuals with severe mental illnesses who refuse to take medication voluntarily under any circumstances may require some form of coercion to remain compliant because of anosognosia. Coercive psychiatric treatment is a delicate and complex legal and ethical issue.
One study of voluntary and involuntary inpatients confirmed that committed patients require coercive treatment because they fail to recognize their need for care. The patients committed to the hospital had significantly lower measures of insight than the voluntary patients.
Anosognosia is also closely related to other cognitive dysfunctions that may impair the capacity of an individual to continuously participate in treatment. Other research has suggested that attitudes toward treatment can improve after involuntary treatment and that previously committed patients tend later to seek voluntary treatment.
Reduplicative paramnesia is the delusional belief that a place or location has been duplicated, existing in two or more places simultaneously, or that it has been 'relocated' to another site. It is one of the delusional misidentification syndromes and, although rare, is most commonly associated with acquired brain injury, particularly simultaneous damage to the right cerebral hemisphere and to both frontal lobes.
Klüver–Bucy syndrome is a syndrome resulting from bilateral lesions of the medial temporal lobe (including amygdaloid nucleus). Klüver–Bucy syndrome may present with compulsive eating, hypersexuality, insertion of inappropriate objects in the mouth (hyperorality), visual agnosia, and .
There is no cure for Gerstmann syndrome. Treatment is symptomatic and supportive. Occupational and speech therapies may help diminish the dysgraphia and apraxia. In addition, calculators and word processors may help school children cope with the symptoms of the disorder.
Topographical disorientation, also known as topographical agnosia and topographagnosia, is the inability to orient oneself in one's surroundings as a result of focal brain damage. This disability may result from the inability to make use of selective spatial information (e.g., environmental landmarks) or to orient by means of specific cognitive strategies such as the ability to form a mental representation of the environment, also known as a cognitive map. It may be part of a syndrome known as visuospatial dysgnosia.
Once it has been positively identified, pharmacotherapy follows. Antipsychotic drugs are the frontrunners in treatment for Fregoli and other DMSs. In addition to antipsychotics, anticonvulsants and antidepressants are also prescribed in some treatment courses. If a Fregoli patient has other psychological disorders, treatment often results in the use of trifluoperazine.
Intoxication accounts for a small percentage of musical hallucination cases. Intoxication leads to either withdrawal or inflammatory encephalopathy, which are major contributors to musical hallucinations. Some of the drugs that have been found to relate to musical hallucinations include salicylates, benzodiazepines, pentoxifylline, propranolol, clomipramine, amphetamine, quinine, imipramine, a phenothiazine, carbamazepine, marijuana, paracetamol, phenytoin, procaine, and alcohol. General anesthesia has also been association with musical hallucinations.
In a case study by Gondim et al. 2010, a seventy–seven-year-old woman with Parkinson's disease (PD) was administered amantadine after a year of various other antiparkinsonian treatments. Two days into her treatment, she started to experience musical hallucinations, which consisted of four musical pieces. The music persisted until three days after cessation of the drug. Although the patient was taking other medications at the same time, the timing of onset and offset suggested that amantadine either had a synergistic effect with the other drugs or simply caused the hallucinations. Although the case wasn't specific to intoxication, it leads to the idea that persons with PD who are treated with certain drugs can experience musical hallucinations.
Musicogenic epilepsy is a form of reflex epilepsy with seizures elicited by special stimuli.
It has probably been described for the first time in 1605 by the French philosopher and scholar Joseph Justus Scaliger (1540-1609). Later publications were, in the eighteenth century, among others, by the German physician Samuel Schaarschmidt, in the nineteenth century 1823 by the British physician John C. Cooke, 1881 by the British neurologist and epileptologist William Richard Gowers, as well as in 1913 by the Russian neurologist, clinical neurophysiologist and psychiatrist Vladimir Mikhailovich Bekhterev. In 1937 the British neurologist Macdonald Critchley coined the term for the first time and classified it as a form of reflex epilepsy.
Most patients have temporal lobe epilepsy. Listening, probably also thinking or playing, of usually very specific music with an emotional content triggers focal seizures with or without loss of awareness, occasionally also evolving to bilateral tonic-clonic seizures.
Although musicality is at least in non-musicians predominantly located in the right temporal lobe, the seizure onset may also be left-hemispherical. Of the approximately 100 patients reported in the literature so far, about 75% had temporal lobe epilepsy, women were slightly more affected, and the mean age of onset was about 28 years. Ictal EEG and SPECT findings as well as functional MRI studies localized the epileptogenic area predominantly in the right temporal lobe. Treatment with epilepsy surgery leading to complete seizure freedom has been reported.
To date, there is no successful method of treatment that "cures" musical hallucinations. There have been successful therapies in single cases that have ameliorated the hallucinations. Some of these successes include drugs such as neuroleptics, antidepressants, and certain anticonvulsive drugs. A musical hallucination was alleviated, for example, by antidepressant medications given to patients with depression. Sanchez reported that some authors have suggested that the use of hearing aids may improve musical hallucination symptoms. They believed that the external environment influences the auditory hallucinations, showing worsening of symptoms in quieter environments than in noisier ones. Oliver Sacks' patient, Mrs. O'C, reported being in an "ocean of sound" despite being in a quiet room due to a small thrombosis or infarction in her right temporal lobe. After treatment, Mrs. O'C was relinquished of her musical experience but said that, "I do miss the old songs. Now, with lots of them, I can't even recall them. It was like being given back a forgotten bit of my childhood again." Sacks also reported another elderly woman, Mrs. O'M, who had a mild case of deafness and reported hearing musical pieces. When she was treated with anticonvulsive medications, her musical hallucinations ceased but when asked if she missed them, she said "Not on your life."
Focal seizures (also called partial seizures and localized seizures) are seizures which affect initially only one hemisphere of the brain. The brain is divided into two hemispheres, each consisting of four lobes – the frontal, temporal, parietal and occipital lobes. A focal seizure is generated in and affects just one part of the brain – a whole hemisphere or part of a lobe. Symptoms will vary according to where the seizure occurs. In the frontal lobe symptoms may include a wave-like sensation in the head; in the temporal lobe, a feeling of déjà vu; in the parietal lobe, a numbness or tingling; and in the occipital lobe, visual disturbance or hallucination.
There is currently no known curative treatment for SD. The average duration of illness is 8–10 years, and its progression cannot be slowed. Progression of SD can lead to behavioral and social difficulties, thus supportive care is essential for improving quality of life in SD patients as they grow more incomprehensible.
Continuous practice in lexical learning has been shown to improve semantic memory in SD patients.
SD has no known preventative measures.
Geschwind syndrome, also known as Gastaut-Geschwind, is a group of behavioral phenomena evident in some people with temporal lobe epilepsy. It is named for one of the first individuals to categorize the symptoms, Norman Geschwind, who published prolifically on the topic from 1973 to 1984. There is controversy surrounding whether it is a true neuropsychiatric disorder. Temporal lobe epilepsy causes chronic, mild, interictal (i.e. between seizures) changes in personality, which slowly intensify over time. Geschwind syndrome includes five primary changes; hypergraphia, hyperreligiosity, atypical (usually reduced) sexuality, circumstantiality, and intensified mental life. Not all symptoms must be present for a diagnosis. Only some people with epilepsy or temporal lobe epilepsy show features of Geschwind syndrome.
Specific and accepted scientific treatment for PCA has yet to be discovered; this may be due to the rarity and variations of the disease. At times PCA patients are treated with prescriptions originally created for treatment of AD such as, cholinesterase inhibitors, Donepezil, Rivastigmine and Galantamine, and Memantine. Antidepressant drugs have also provided some positive effects.
Patients may find success with non-prescription treatments such as psychological treatments. PCA patients may find assistance in meeting with an occupational therapist or sensory team for aid in adapting to the PCA symptoms, especially for visual changes. People with PCA and their caregivers are likely to have different needs to more typical cases of Alzheimer's disease, and may benefit from specialized support groups such as the PCA Support Group based at University College London, or other groups for young people with dementia. No study to date has been definitive to provide accepted conclusive analysis on treatment options.
As of 2014, no clinical trials had been conducted to determine what treatments are safe and effective; a few case reports had been published describing treatment of small numbers of people (two to twelve per report) with clomipramine, flunarizine, nifedipine, topiramate, carbamazepine, methylphenidate. Studies suggest that education and reassurance can reduce the frequency of EHS episodes. There is some evidence that individuals with EHS rarely report episodes to medical professionals.