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.

Lorazepam and clonazepam are front line treatment for severe convulsions, belonging to the benzodiazepine class of medications.

Anticonvulsants are the most successful medication in reducing and preventing seizures from reoccurring. The goal of these medications in being able to reduce the reoccurrence of seizures is to be able to limit the amount of rapid and extensive firing of neurons so that a focal region of neurons cannot become over-activated thereby initiating a seizure. Although anticonvulsants are able to reduce the amount of seizures that occur in the brain, no medication has been discovered to date that is able to prevent the development of epilepsy following a head injury. There are a wide range of anticonvulsants that have both different modes of action and different abilities in preventing certain types of seizures. Some of the anticonvulsants that are prescribed to patients today include: Carbamazepine (Tegretol), Phenytoin (Dilantin Kapseals), Gabapentin (Neurontin), Levetiracetam (Keppra), Lamotrigine (Lamictal), Topiramate (Topamax), Tiagabine (Gabitril), Zonisamide (Zonegran) and Pregabalin (Lyrica).

Where surgery is not recommended, further management options include new (including experimental) anticonvulsants, and vagus nerve stimulation. The ketogenic diet is also recommended for children, and some adults. Other options include brain cortex responsive neural stimulators, deep brain stimulation, stereotactic radiosurgery, such as the gamma knife, and laser ablation.

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.

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 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.

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 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.

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.

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.

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."

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.

Treatment of Foix–Chavany–Marie syndrome depends on the onset of symptoms and involves a multidisciplinary approach. Drugs are used in neurological recovery depending on the etiological classification of FCMS. FCMS caused by epilepsy, specifically resulting in the development of lesions in the bilateral and subcortical regions of the brain can be treated using antiepileptic drugs to reverse abnormal EEG changes and induce complete neurological recovery. In addition, a hemispherectomy can be performed to reverse neurological deficits and control the seizures. This procedure can result in a complete recovery from epileptic seizures. Physical therapy is also used to manage symptoms and improve quality of life. Classical FCMS resulting in the decline of ones ability to speak and swallow can be treated using neuromuscular electrical stimulation and traditional dysphagia therapy. Speech therapy further targeting dysphagia can strengthen oral musculature using modified feeding techniques and postures. Therapeutic feedings include practicing oral and lingual movements using ice chips. In addition, different procedures can be performed by a neurosurgeon to alleviate some symptoms.

In the 1960s it was discovered that when medium-chain triglycerides (MCT) fats are metabolized in the body more ketone bodies are produced then from metabolizing any other fat. Based on this mechanism the MCT ketogenic diet a modification of the ketogenic diet was developed and it has nearly replaced the classic ketogenic diet in the USA. In the MCT ketogenic diet MCT oil is added to ketogenic meals, which allows the carbohydrate content to be increased to around 15 to 20%. This way some patients find the meals more enjoyable. The success rate of the MCT ketogenic diet does not differ from the classic ketogenic diet however not all children can tolerate the necessary large amounts of MCT oil which is also very expensive.

Many forms of amnesia fix themselves without being treated. However, there are a few ways to cope with memory loss if that is not the case. One of these ways is cognitive or occupational therapy. In therapy, amnesiacs will develop the memory skills they have and try to regain some they have lost by finding which techniques help retrieve memories or create new retrieval paths. This may also include strategies for organizing information to remember it more easily and for improving understanding of lengthy conversation.

Another coping mechanism is taking advantage of technological assistance, such as a personal digital device to keep track of day-to-day tasks. Reminders can be set up for appointments, when to take medications, birthdays and other important events. Many pictures can also be stored to help amnesiacs remember names of friends, family and co-workers. Notebooks, wall calendars, pill reminders and photographs of people and places are low-tech memory aids that can help as well.

While there are no medications available to treat amnesia, underlying medical conditions can be treated to improve memory. Such conditions include but are not limited to low thyroid function, liver or kidney disease, stroke, depression, bipolar disorder and blood clots in the brain. Wernicke–Korsakoff syndrome involves a lack of thiamin and replacing this vitamin by consuming thiamin-rich foods such as whole-grain cereals, legumes (beans and lentils), nuts, lean pork, and yeast. Treating alcoholism and preventing alcohol and illicit drug use can prevent further damage, but in most cases will not recover lost memory.

Although improvements occur when patients receive certain treatments, there is still no actual cure remedy for amnesia so far. To what extent the patient recovers and how long the amnesia will continue depends on the type and severity of the lesion.

Treatment varies for micropsia due to the large number of different causes for the condition.

Treatments involving the occlusion of one eye and the use of a prism fitted over an eyeglass lens have both been shown to provide relief from micropsia.

Micropsia that is induced by macular degeneration can be treated in several ways. A study called AREDS (age-related eye disease study) determined that taking dietary supplements containing high-dose antioxidants and zinc produced significant benefits with regard to disease progression. This study was the first ever to prove that dietary supplements can alter the natural progression and complications of a disease state. Laser treatments also look promising but are still in clinical stages.

The primary means of treating auditory hallucinations is antipsychotic medications which affect dopamine metabolism. If the primary diagnosis is a mood disorder (with psychotic features), adjunctive medications are often used (e.g., antidepressants or mood stabilizers). These medical approaches may allow the person to function normally but are not a cure as they do not eradicate the underlying thought disorder.

In a confirmed medical diagnosis, therapy is used to isolate and begin treating the cause of the disorder. Thereafter, psychiatric medication is used a secondary step in treatment. Medications include antipsychotic, antidepressant, or sedation-inducing, varying on the patients severity.

Treatment of psychorganic syndrome is directed at the main disease. Nootropics like piracetam, have had positive effects on patients. Vitamin therapy, antioxidants, neurotropic, and cerebroprotective have also found to be effective when put on a repeat course.

Several drug therapies have been used on patients with KLS, but none of them have been subject to randomized controlled trials. A 2016 Cochrane Review concluded that "No evidence indicates that pharmacological treatment for Kleine-Levin syndrome is effective and safe".

In several cases, stimulants, including modafinil, have been reported to have a limited effect on patients, often alleviating sleepiness. They can cause behavioral problems, but they may pose fewer issues if used in older patients with mild symptoms. In some case reports, lithium has been reported to decrease the length of episodes and the severity of their symptoms and to increase the time between episodes. It has been reported to be effective in about 25 to 60 percent of cases. Its use carries the risk of side effects in the thyroid or kidneys. Anti-psychotics and benzodiazepines can help alleviate psychotic and anxiety related symptoms, respectively. Carbamazepine has been reported to be less effective than lithium but more effective than some drugs in its class. Electroconvulsive therapy is not effective and worsens symptoms.

KLS patients generally do not need to be admitted to hospitals. It is recommended that caregivers reassure them and encourage them to maintain sleep hygiene. It may also be necessary for patients to be prevented from putting themselves in dangerous situations, such as driving.

Approaches used to treat those who suffer from anterograde amnesia often use interventions which focus on compensatory techniques, such as beepers, written notes, diaries or through intensive training programs involving the active participation of the individual concerned, along with their supporting network of family and friends.

In this perspective, environmental adaptation techniques are used, such as the compensatory technique education to training (exercise), organizational strategies, visual imagery and verbal labeling. In addition, other techniques are also used in rehabilitation, such as implicit tasks, speech and mnemotechnic methods.

So far, it has been proven that education techniques of compensatory strategies for memory disorders are effective in individuals with minor traumatic brain injuries. In moderately or severely injured individuals, effective interventions are those appealing to external aids, such as reminders in order to facilitate particular knowledge or skill acquisition. Reality orientation techniques are also considered; Their purpose is to enhance orientation using stimulation and repetition of the basic orientation information. These techniques are regularly applied in populations of patients primarily presenting with dementia and head-injured patients.

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.

Individual therapy may be best suited to treat the individual's delusions. Persistence is needed in establishing a therapeutic empathy without validating the patient’s delusional system or overtly confronting the system. Cognitive techniques that include reality testing and reframing can be used. Antipsychotics and other therapeutic drugs have been used with relative success.

Prisms or "field expanders" that bend light have been prescribed for decades in patients with hemianopsia. Higher power Fresnel ("stick-on") prisms are commonly employed because they are thin and light weight, and can be cut and placed in different positions on a spectacle lens.

Peripheral prism spectacles expand the visual field of patients with hemifield visual defects and have the potential to improve visual function and mobility. Prism spectacles incorporate higher power prisms, with variable shapes and designs. The Gottlieb button prism, and the Peli superior and inferior horizontal bands are some proprietary examples of prism glasses. These high power prisms "create" artificial peripheral vision into the non-blind field for obstacle avoidance and motion detection.

Treatment for confabulation is somewhat dependent on the cause or source, if identifiable. For example, treatment of Wernicke–Korsakoff syndrome involves large doses of vitamin B in order to reverse the thiamine deficiency. If there is no known physiological cause, more general cognitive techniques may be used to treat confabulation. A case study published in 2000 showed that Self-Monitoring Training (SMT) reduced delusional confabulations. Furthermore, improvements were maintained at a three-month follow-up and were found to generalize to everyday settings. Although this treatment seems promising, more rigorous research is necessary to determine the efficacy of SMT in the general confabulation population.