Reactive strategies include:

- Redirection: distracting the person by offering another activity, or changing the topic of conversation. Offer the person a choice of 2 or 3 things, but no more than 3, because this can be overwhelming. In offering a choice, make sure to pause to allow the person time to process the information and give a response.

- Talking to the person and finding out what the problem is

- Working out what the person's behaviour is trying to communicate

- Crisis management

Positive Behaviour Support (PBS) is a treatment approach that looks at the best way to work with each individual with disabilities. A behavioural therapist conducts a functional analysis of behaviour which helps to determine ways to improve the quality of life for the person and does not just deal with problem behaviour.

PBS also acknowledges the needs of support staff and includes strategies to manage crises when they arise. The following model is a brief guide to staff to remind them of key things to think about when planning support for a person with disabilities. There are two main objectives: reacting situationally when the behaviour occurs, and then acting proactively to prevent the behaviour from occurring.

Dextromethorphan hydrobromide is a generic drug that affects the signals in the brain that trigger the cough reflex. It is generally used as a cough suppressant, although it can sometimes be used, medicinally, as a pain reliever, and is also used as a recreational drug. "Dextromethorphan (DM) is a sigma-1 receptor agonist and an uncompetitive NMDA receptor antagonist."

Quinidine sulfate affects the way the heart beats, and is generally used in people with certain heart rhythm disorders. It is also used to treat malaria. Quinidine sulfate, as a metabolic inhibitor, "increases plasma levels of dextromethorphan by competitively inhibiting cytochrome P450 2D6, which catalyzes a major biotransformation pathway for dextromethorphan," enabling therapeutic dextromethorphan concentrations.

Nuedexta is a patented combination of these two generic drugs, and is the first FDA-approved drug for the treatment of PBA, approved on October 29, 2010. In December 2007, clinical study information for Nuedexta was first submitted to ClinicalTrials.gov, (a Web-based resource maintained by the National Library of Medicine (NLM) at the National Institutes of Health (NIH)). Sponsored by Avanir Pharmaceuticals, (with brief title, "Safety and Efficacy of AVP-923 in PBA Patients With ALS or MS"), the study was assigned NCT Number NCT00573443. Final updates and verifications occurred in June 2013 on the ClinicalTrials.gov site.

For this multicenter study, the "Objectives...[were] to evaluate the safety, tolerability, and efficacy of two different doses of AVP-923 [Dextromethorphan/quinidine combination]...when compared to placebo." The conditions and results of that study are as follows:

Other studies have confirmed the results of NCT00573443, but, "The mechanism by which dextromethorphan exerts therapeutic effects in patients with pseudobulbar affect is unknown."

The current treatments for CCAS focus on relieving the symptoms. One treatment is a cognitive-behavioral therapy (CBT) technique that involves making the patient aware of his or hers cognitive problems. For example, many CCAS patients struggle with multitasking. With CBT, the patient would have to be aware of this problem and focus on just one task at a time. This technique is also used to relieve some motor symptoms. In a case study with a patient who had a stroke and developed CCAS, improvements in mental function and attention were achieved through reality orientation therapy and attention process training. Reality orientation therapy consists of continually exposing the patient to stimuli of past events, such as photos. Attention process training consists of visual and auditory tasks that have been shown to improve attention. The patient struggled in applying these skills to “real-life” situations. It was the help of his family at home that significantly helped him regain his ability to perform activities of daily living. The family would motivate the patient to perform basic tasks and made a regular schedule for him to follow.

Transcranial magnetic stimulation (TMS) has also been proposed to be a possible treatment of psychiatric disorders of the cerebellum. One study used TMS on the vermis of patients with schizophrenia. After stimulation, the patients showed increased happiness, alertness and energy, and decreased sadness. Neuropsychological testing post-stimulation showed improvements in working memory, attention, and visual spatial skill. Another possible method of treatment for CCAS is doing exercises that are used to relieve the motor symptoms. These physical exercises have been shown to also help with the cognitive symptoms.

Medications that help relieve deficits in traumatic brain injuries in adults have been proposed as candidates to treat CCAS. Bromocriptine, a direct D2 agonist, has been shown to help with deficits in executive function and spatial learning abilities. Methylphendiate has been shown to help with deficits in attention and inhibition. Neither of these drugs has yet been tested on a CCAS population. It may also be that some of the symptoms of CCAS improve over time without any formal treatment. In the original report of CCAS, four patients with CCAS were re-examined one to nine months after their initial neuropsychological evaluation. Three of the patients showed improvement in deficits without any kind of formal treatment, though executive function was still found to be one standard deviation below average. In one patient, the deficits worsened over time. This patient had cerebellar atrophy and worsened in visual spatial abilities, concept formation, and verbal memory. It should be noted that none of these treatments were tested on a large enough sample to determine if they would help with the general CCAS population. Further research needs to be done on treatments for CCAS.

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.

Treatments using intravenous magnesium sulfate have shown to reduce the symptoms of akinetic mutism. In one case, a 59-year-old woman was administered intravenous magnesium sulfate in an attempt to resolve her akinetic mutism. The patient was given 500 mg of magnesium every eight hours, and improvement was seen after 24 hours. She became more verbal and attentive, and treatment was increased to 1000 mg every eight hours as conditions continued to improve.

Cognitive-behavioural therapy (CBT) is a frequently suggested treatment for executive dysfunction, but has shown limited effectiveness. However, a study of CBT in a group rehabilitation setting showed a significant increase in positive treatment outcome compared with individual therapy. Patients' self-reported symptoms on 16 different ADHD/executive-related items were reduced following the treatment period.

Some patients have been treated by injecting botulinum toxin (botox) near the vocal cords. This does not prevent the vocalizations, but the partial paralysis that results helps to control the volume of any outbursts. Surprisingly, botox injections result in more generalized relief of tics than the vocal relief expected.

The severity and frequency of outbursts can also be decreased by surgically disabling nuclei in the thalamus, the globus pallidus and the cingulate cortex.

In terms of treatment for frontal lobe disorder, general supportive care is given, also some level of supervision could be needed. The prognosis will depend on the cause of the disorder, of course. A possible complication is that individuals with severe injuries may be disabled, such that, a caregiver may be unrecognizable to the person.

Another aspect of treatment of frontal lobe disorder is speech therapy. This type of therapy might help individuals with symptoms that are associated with aphasia and dysarthria.

There is much research that needs to be conducted on CCAS. A necessity for future research is to conduct more longitudinal studies in order to determine the long-term effects of CCAS. One way this can be done is by studying cerebellar hemorrhage that occurs during infancy. This would allow CCAS to be studied over a long period to see how CCAS affects development. It may be of interest to researchers to conduct more research on children with CCAS, as the survival rate of children with tumors in the cerebellum is increasing. Hopefully future research will bring new insights on CCAS and develop better treatments.

Education of patients, families, and caregivers is an important component of the appropriate treatment of PBA. Crying associated with PBA may be incorrectly interpreted as depression; laughter may be embarrassing. It is therefore critical for families and caregivers to recognize the pathological nature of PBA and the reassurance that this is an involuntary syndrome that is manageable.

Traditionally, antidepressants such as sertraline, fluoxetine,citalopram, nortriptyline and amitriptyline have been prescribed with some efficacy.

As seen in the case of Elsie Nicks, the puncture or removal of a cyst causing akinetic mutism can relieve symptoms almost immediately. However, if the cyst fills up again, the symptoms can reappear.

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.

One subsequent human study found no effects of vasopressin on memory. The nonsignificant results were attributed to the study's many potential flaws, particularly its small sample size, the inability of vasopressin to penetrate the blood brain barrier when administered as a nasal spray, inadequate dosing and differences in severity of head injury between the samples. However, Eames et al. (1999) found statistically significant improvements on several tests of memory with the use of a vasopressin nasal spray, with no reported ill effects. Although the degree of improvement was mild, and it could be attributed to numerous other factors of the rehabilitative program, the lack of any ill effects suggests that vasopressin is, at the least, a possible enhancement for a treatment regimen.

Lithium is the only drug that appears to have a preventive effect. In two studies of more than 100 patients, lithium helped prevent recurrence of symptoms in 20% to 40% of cases. The recommended blood level of lithium for KLS patients is 0.8-1.2 mEq/ml. It is not known if other mood stabilizers have an effect on the condition. Anti-depressants do not prevent recurrence.

There is no cure for the alien hand syndrome. However, the symptoms can be reduced and managed to some degree by keeping the alien hand occupied and involved in a task, for example by giving it an object to hold in its grasp. Specific learned tasks can restore voluntary control of the hand to a significant degree. One patient with the "frontal" form of alien hand who would reach out to grasp onto different objects (e.g., door handles) as he was walking was given a cane to hold in the alien hand while walking, even though he really did not need a cane for its usual purpose of assisting with balance and facilitating ambulation. With the cane firmly in the grasp of the alien hand, it would generally not release the grasp and drop the cane in order to reach out to grasp onto a different object. Other techniques proven to be effective includes; wedging the hand between the legs or slapping it; warm water application and visual or tactile contact. Additionally, Wu et al. found that an irritating alarm activated by biofeedback reduced the time the alien hand held an object.

In the presence of unilateral damage to a single cerebral hemisphere, there is generally a gradual reduction in the frequency of alien behaviors observed over time and a gradual restoration of voluntary control over the affected hand. Actually, when AHS originates from focal injury of acute onset, recovery usually occurs within a year. One theory is that neuroplasticity in the bihemispheric and subcortical brain systems involved in voluntary movement production can serve to re-establish the connection between the executive production process and the internal self-generation and registration process. Exactly how this may occur is not well understood, but a process of gradual recovery from alien hand syndrome when the damage is confined to a single cerebral hemisphere has been reported. In some instances, patients may resort to constraining the wayward, undesirable and sometimes embarrassing actions of the impaired hand by voluntarily grasping onto the forearm of the impaired hand using the intact hand. This observed behavior has been termed "self-restriction" or "self-grasping".

In another approach, the patient is trained to perform a specific task, such as moving the alien hand to contact a specific object or a highly salient environmental target, which is a movement that the patient can learn to generate voluntarily through focused training in order to effectively override the alien behavior. It is possible that some of this training produces a re-organization of premotor systems within the damaged hemisphere, or, alternatively, that ipsilateral control of the limb from the intact hemisphere may be expanded.

Another method involves simultaneously "muffling" the action of the alien hand and limiting the sensory feedback coming back to the hand from environmental contact by placing it in a restrictive "cloak" such as a specialized soft foam hand orthosis or, alternatively, an everyday oven mitt. Other patients have reported using an orthotic device to restrict perseverative grasping or restraining the alien hand by securing it to the bed pole. Of course, this can limit the degree to which the hand can participate in addressing functional goals for the patient and may be considered to be an unjustifiable restraint.

Theoretically, this approach could slow down the process through which voluntary control of the hand is restored if the neuroplasticity that underlies recovery involves the recurrent exercise of voluntary will to control the actions of the hand in a functional context and the associated experiential reinforcement through successful willful suppression of the alien behavior.

Treatment for OCPD includes psychotherapy, cognitive behavioral therapy, behavior therapy or self-help. Medication may be prescribed. In behavior therapy, a person with OCPD discusses with a psychotherapist ways of changing compulsions into healthier, productive behaviors. Cognitive analytic therapy is an effective form of behavior therapy.

Treatment is complicated if the person does not accept that they have OCPD, or believes that their thoughts or behaviors are in some sense correct and therefore should not be changed. Medication alone is generally not indicated for this personality disorder. Selective serotonin reuptake inhibitors (SSRIs) may be useful in addition to psychotherapy by helping the person with OCPD be less bogged down by minor details, and to lessen how rigid they are.

People with OCPD are three times more likely to receive individual psychotherapy than people with major depressive disorder. There are higher rates of primary care utilization. There are no known properly controlled studies of treatment options for OCPD. More research is needed to explore better treatment options.

Selective serotonin reuptake inhibitors (SSRIs) and serotonin-norepinephrine reuptake inhibitors (SNRIs) may have some benefit for PTSD symptoms. Tricyclic antidepressants are equally effective but are less well tolerated. Evidence provides support for a small or modest improvement with sertraline, fluoxetine, paroxetine, and venlafaxine. Thus, these four medications are considered to be first-line medications for PTSD.

Early research pointed to vasopressin as a potential treatment for improving the memory of patients living with post-traumatic amnesia (PTA). Lysine vasopressin, a modified form of the vasopressin molecule, had positive effects on memory when administered by injection to patients with amnesia resulting from traumatic brain injury and Korsakoff's syndrome. Subsequent animal studies with rats found similar results, particularly in aversion and avoidance learning tasks. Rats lacking adequate vasopressin, either due to genetic defect or hypophysectomy (surgical removal of the pituitary gland), exhibited significant improvements in memory and learning functions when exogenous vasopressin was administered. Particularly encouraging was the finding that a short treatment period produced long-lasting improvements, in both humans and rats. However, the animal models of PTA are highly limited, as the dimension of self-awareness and orientation is almost impossible to model adequately. PTA in animals, especially rats, is often observed post-trauma (commonly post-surgery), but it is often only measured in terms of impaired learning or unusual behavior.

Since 1997 there has been experimental and clinical practice of psychosocial treatment for adults with executive dysfunction, and particularly attention-deficit/hyperactivity disorder (ADHD). Psychosocial treatment addresses the many facets of executive difficulties, and as the name suggests, covers academic, occupational and social deficits. Fifty percent of medication-based treatments for adults with ADHD are ineffective, so psychosocial treatment—although complicated and difficult to apply—is a promising alternative. Psychosocial treatment facilitates marked improvements in major symptoms of executive dysfunction such as time management, organization and self-esteem.

Benzodiazepines are not recommended for the treatment of PTSD due to a lack of evidence of benefit and risk of worsening PTSD symptoms. Some authors believe that the use of benzodiazepines is contraindicated for acute stress, as this group of drugs promotes dissociation and ulterior revivals. Nevertheless, some use benzodiazepines with caution for short-term anxiety and insomnia. While benzodiazepines can alleviate acute anxiety, there is no consistent evidence that they can stop the development of PTSD and may actually increase the risk of developing PTSD 2–5 times. Additionally, benzodiazepines may reduce the effectiveness of psychotherapeutic interventions, and there is some evidence that benzodiazepines may actually contribute to the development and chronification of PTSD. For those who already have PTSD, benzodiazepines may worsen and prolong the course of illness, by worsening psychotherapy outcomes, and causing or exacerbating aggression, depression (including suicidality), and substance use. Drawbacks include the risk of developing a benzodiazepine dependence, tolerance (i.e., short-term benefits wearing off with time), and withdrawal syndrome; additionally, individuals with PTSD (even those without a history of alcohol or drug misuse) are at an increased risk of abusing benzodiazepines. Due to a number of other treatments with greater efficacy for PTSD and less risks (e.g., prolonged exposure, cognitive processing therapy, eye movement desensitization and reprocessing, cognitive restructuring therapy, trauma-focused cognitive behavioral therapy, brief eclectic psychotherapy, narrative therapy, stress inoculation training, serotonergic antidepressants, adrenergic inhibitors, antipsychotics, and even anticonvulsants), benzodiazepines should be considered relatively contraindicated until all other treatment options are exhausted. For those who argue that benzodiazepines should be used sooner in the most severe cases, the adverse risk of disinhibition (associated with suicidality, aggression and crimes) and clinical risks of delaying or inhibiting definitive efficacious treatments, make other alternative treatments preferable (e.g., inpatient, residential, partial hospitalization, intensive outpatient, dialectic behavior therapy; and other fast-acting sedating medications such as trazodone, mirtazapine, amitripytline, doxepin, prazosin, propranolol, guanfacine, clonidine, quetiapine, olanzapine, valproate, gabapentin).

Before prescribing medication for these conditions which often resolve spontaneously, recommendations have pointed to improved skin hygiene, good hydration via fluids, good nutrition, and installation of padded bed rails with use of proper mattresses. Pharmacological treatments include the typical neuroleptic agents such as fluphenazine, pimozide, haloperidol and perphenazine which block dopamine receptors; these are the first line of treatment for hemiballismus. Quetiapine, sulpiride and olanzapine, the atypical neuroleptic agents, are less likely to yield drug-induced parkinsonism and tardive dyskinesia. Tetrabenazine works by depleting presynaptic dopamine and blocking postsynaptic dopamine receptors, while reserpine depletes the presynaptic catecholamine and serotonin stores; both of these drugs treat hemiballismus successfully but may cause depression, hypotension and parkinsonism. Sodium valproate and clonazepam have been successful in a limited number of cases. Stereotactic ventral intermediate thalamotomy and use of a thalamic stimulator have been shown to be effective in treating these conditions.

The medical treatment of essential tremor at the Movement Disorders Clinic at Baylor College of Medicine begins with minimizing stress and tremorgenic drugs along with recommending a restricted intake of beverages containing caffeine as a precaution, although caffeine has not been shown to significantly intensify the presentation of essential tremor. Alcohol amounting to a blood concentration of only 0.3% has been shown to reduce the amplitude of essential tremor in two-thirds of patients; for this reason it may be used as a prophylactic treatment before events during which one would be embarrassed by the tremor presenting itself. Using alcohol regularly and/or in excess to treat tremors is highly unadvisable, as there is a purported correlation between tremor and alcoholism. Alcohol is thought to stabilize neuronal membranes via potentiation of GABA receptor-mediated chloride influx. It has been demonstrated in essential tremor animal models that the food additive 1-octanol suppresses tremors induced by harmaline, and decreases the amplitude of essential tremor for about 90 minutes.

Two of the most valuable drug treatments for essential tremor are propranolol, a beta blocker, and primidone, an anticonvulsant. Propranolol is much more effective for hand tremor than head and voice tremor. Some beta-adrenergic blockers (beta blockers) are not lipid-soluble and therefore cannot cross the blood–brain barrier (propranolol being an exception), but can still act against tremors; this indicates that this drug’s mechanism of therapy may be influenced by peripheral beta-adrenergic receptors. Primidone’s mechanism of tremor prevention has been shown significantly in controlled clinical studies. The benzodiazepine drugs such as diazepam and barbiturates have been shown to reduce presentation of several types of tremor, including the essential variety. Controlled clinical trials of gabapentin yielded mixed results in efficacy against essential tremor while topiramate was shown to be effective in a larger double-blind controlled study, resulting in both lower Fahn-Tolosa-Marin tremor scale ratings and better function and disability as compared to placebo.

It has been shown in two double-blind controlled studies that injection of botulinum toxin into muscles used to produce oscillatory movements of essential tremors, such as forearm, wrist and finger flexors, may decrease the amplitude of hand tremor for approximately three months and that injections of the toxin may reduce essential tremor presenting in the head and voice. The toxin also may help tremor causing difficulty in writing, although properly adapted writing devices may be more efficient. Due to high incidence of side effects, use of botulinum toxin has only received a C level of support from the scientific community.

Deep brain stimulation toward the ventral intermediate nucleus of the thalamus and potentially the subthalamic nucleus and caudal zona incerta nucleus have been shown to reduce tremor in numerous studies. That toward the ventral intermediate nucleus of the thalamus has been shown to reduce contralateral and some ipsilateral tremor along with tremors of the cerebellar outflow, head, resting state and those related to hand tasks; however, the treatment has been shown to induce difficulty articulating thoughts (dysarthria), and loss of coordination and balance in long-term studies. Motor cortex stimulation is another option shown to be viable in numerous clinical trials.

Witzelsucht (from the German "witzeln", meaning to joke or wisecrack, and "sucht", meaning addiction or yearning) is a set of rare neurological symptoms characterized by a tendency to make puns, or tell inappropriate jokes or pointless stories in socially inappropriate situations. A less common symptom is hypersexuality, the tendency to make sexual comments at inappropriate times or situations. Patients do not understand that their behavior is abnormal, therefore are nonresponsive to others' reactions. This disorder is most commonly seen in patients with frontal lobe damage, particularly right frontal lobe tumors or trauma. The disorder remains named in accordance with its reviewed definition by German neurologist Hermann Oppenheim; its first description as the less focused "Moria" ("stupidity"), by German neurologist Moritz Jastrowitz, was in 1888.

Due to similarity of symptoms of the disorder to the mannerisms of Batman's arch-rival Joker, it is sometimes known as 'The Joker Syndrome'

Lesionsing is the intentional destruction of neuronal cells in a particular area used for therapeutic purposes. Though this seems dangerous, vast improvements have been achieved in patients with movement disorders. The exact process generally involves unilateral lesioning in the sensorimotor territory of the GPi. This process is called pallidotomy. It is believed that the success of pallidotomies in reducing the effects of movement disorders may result from the interruption of abnormal neuronal activity in the GPi. This ablation technique can be viewed as simply removing a faulty piece of a circuit. With the damaged piece of the circuit removed, the healthy area of the circuit can continue normal function.