Original Article
Dement Neuropsychol 2013 September;7(3):269-277 BPSD following traumatic brain injury
Renato Anghinah1, Fabio Rios Freire1, Fernanda Coelho1, Juliana Rhein Lacerda1, Magali Taino Schmidt1, Vanessa Tomé Gonçalves Calado1, Jéssica Natuline Ianof1, Sergio Machado2, Bruna Velasques3, Pedro Ribeiro4, Luis Fernando Hindi Basile5, Wellingson Silva Paiva6, Robson Luis Amorim6 ABStrAct. Annually, 700,000 people are hospitalized with brain injury acquired after traumatic brain injury (TBI) in Brazil.
Objective: We aim to review the basic concepts related to TBI, and the most common Behavioral and Psychological
Symptoms of Dementia (BPSD) findings in moderate and severe TBI survivors. We also discussed our strategies used
to manage such patients in the post-acute period. Methods: Fifteen TBI outpatients followed at the Center for Cognitive
Rehabilitation Post-TBI of the Clinicas Hospital of the University of São Paulo were submitted to a neurological, neuro-
psychological, speech and occupational therapy evaluation, including the Mini-Mental State Examination. Rehabilitation
strategies will then be developed, together with the interdisciplinary team, for each patient individually. Where necessary,
the pharmacological approach wil be adopted. Results: Our study wil discuss options of pharmacologic treatment choices
for cognitive, behavioral, or affective disorders following TBI, providing relevant information related to a structured cognitive
rehabilitation service and certainly will offer an alternative for patients and families afflicted by TBI. Conclusion: Traumatic
brain injury can cause a variety of potentially disabling psychiatric symptoms and syndromes. Combined behavioral and
pharmacological strategies, in the treatment of a set of highly chal enging behavioral problems, appears to be essential for
good patient recovery.
Key words: TBI, traumatic brain injury, BPSD, treatment.
BPSD PóS trAumAtiSmo crAnioencefálico
Anualmente, 700 mil pessoas são hospitalizadas com lesão encefálica adquirida após traumatismo cranioencefálico
(TCE) no Brasil. Objetivo: Nossa meta é revisar os conceitos básicos relacionados ao TCE, e aos Sintomas Comportamentais
e Psicológicos da Demência (BPSD) encontrados nos sobreviventes de TCE moderado e grave. Também discutimos as
estratégias utilizadas para lidar com os pacientes pós-TCE. Métodos: Quinze pacientes ambulatoriais acompanhados no
Centro de Reabilitação Cognitiva pós-traumatismo cranioencefálico do Hospital das Clínicas de São Paulo foram submetidos
a avaliações neurológica, neuropsicológica, fonoaudiológica e de terapia ocupacional, incluindo o mini exame do estado
mental. Em seguida, estratégias de reabilitação serão desenvolvidas, com a equipe multidisciplinar, para cada paciente
individualmente. E, se necessário, a abordagem farmacológica será adotada. Resultados: Nosso estudo irá discutir as
opções de escolha de tratamento farmacológico para desordens cognitivas, comportamentais e afetivas pós-TCE, fornecendo
informações relevantes relacionadas a um serviço de reabilitação cognitiva estruturada e, certamente, irá oferecer uma
alternativa para pacientes e famílias vítimas de TCE. Conclusão: O traumatismo cranioencefálico pode causar uma variedade
de sintomas e síndromes psiquiátricos potencialmente incapacitantes. As estratégias farmacológica e comportamental
combinadas para o tratamento de um conjunto de problemas comportamentais muito desafiador parece ser essencial para
uma boa recuperação do paciente.
Palavras-chave: TCE, traumatismo cranioencefálico, BPSD, tratamento.
to 30% suffer moderate or severe TBI. The Brazilian data indicate that about 700,000 data suggests that 80% of those who suffer mild TBI are able to return to work, whilst 1Center for Cognitive Rehabilitation Post-Traumatic Brain Injury of the Clinicas Hospital of the Division of Neurology, University of São Paulo. 2University Salgado de Oliveira, Niterói, RJ and Panic and Respiration Laboratory, (IPUB/UFRJ). 3 School of Physical Education (EEFD/UFRJ) and National Institute of Traumatology and Orthopaedics (INTO-RJ). 4Laboratory of Brain Mapping and Sensory-Motor Integration (IPUB/UFRJ). 5Psychophysiology Laboratory, Universidade Metodista de São Paulo & High-Resolution EEG Section. 6Division of Neurosurgery, University of São Paulo Medical School.
renato Anghinah. Rua Itacolomi, 333 / cj 83 – 01239-020 São Paulo SP – Brazil. E-mail: [email protected]
Disclosure: The authors report no conflicts of interest. Received May 07, 2013. Accepted in final form August 02, 2013.
Anghinah R, et al. BPSD and TBI 269 Dement Neuropsychol 2013 September;7(3):269-277 only 20% of moderate and 10% of severe TBI cases can a GCS from 13 to 15, a coma lasting for 20 minutes or less, and a PTA of 1 hour or shorter.
Traumatic brain injury (TBI) is a nondegenerative, Despite the support of the scales, the residual conse- noncongenital insult to the brain from an external me- quences post-TBI will differ in each patient, but the ma- chanical force, potentially leading to permanent or tem- jority who suffer mild trauma have a recovery process porary impairment of cognitive, physical, and psychoso- without major complications, returning to their pre- cial functions, with an associated diminished or altered trauma activities. On the other hand, the majority of patients who suffer moderate and severe TBI will pres- In this context, we will discuss an approach to man- ent sequelae and limitations. However, some patients, age patients with cognitive, behavioral, or affective despite having suffered only mild trauma, have post disorders, rather than define specific pharmacological trauma repercussions that will require special care and treatments, in outpatients followed at the Center for attention from specialized professionals.
Cognitive Rehabilitation Post-Traumatic Brain Injury of Clinicas Hospital of the University of São Paulo, Brazil. most common findings in moderate and severe tBi survivors
The physiological bases for choosing a pharmacological after hospital discharge. This group of patients is charac-
agent to treat such patients, according to the latest re- terized by the diffuse axonal injury and secondary com- search, supports the use of specific drugs for the treat- plication to the site or sites of injury. ment of specific disorders following TBI. After the most critical phase of hospital manage- ment, most patients return home. Although some pa- Severity levels of tBi. The level of consciousness and/or
tients manage to regain some degree of independence in coma in the first 24 hours and the time of Post Trau- their self-care, they are still incapable of applying criti- matic Amnesia (PTA) after the TBI are the most used cal thinking to decision-making processes, providing for references to differentiate them into mild, moderate the needs of their families or continuing work, school or severe injuries. The most widely used method of or social activities, which can cause difficulties in family classifying TBI cases is via a scoring system called the relationships and lead to poor quality of life for patients Glasgow Coma Scale (GCS), which assesses the ability and their relatives. Moreover, these patients may pres- of eye opening, motor and verbal responses as determi- ent with mood alteration and depression.
nants for severity evaluation. GCS scores range from 3 The rehabilitation of these patients after hospital to 15, defining that scores less than or equal to 8 indi- discharge is aimed at a community integration program cate severe injury, from 9 to 12, moderate injury, and with day center resources that provide continuity of pa- tient care so that the individual receives vocational and Post Traumatic Amnesia starts in the period of coma professional training, integrated as part of the rehabili- and lasts until the time when the patient recovers their memory consistently. This period can be associated One of the scales used in our Centre that system- with a transitory state of disorientation, agitation and atically seeks to standardize the functional level of post- behavioral disturbances such as insomnia, agitation, TBI patients and establish the potential of their reha- confabulation and, occasionally, serious affective and bilitation management, is the Rancho Los Amigos levels of cognitive functioning scale.7 This scale is also widely One of the most used scales to evaluate Post Trau- used in many other centers worldwide. In addition, an- matic Amnesia is the GALVESTON Orientation and other scale of diffuse axonal injury rehabilitation stages Amnesia Test. Typically, in post-TBI patients, personal developed by Tuel8 and modified by Katz9 is also quite orientation is recovered before spatial orientation and the perception of what happened. Temporal orientation is the last faculty to be recovered.
most common cognitive impairments following tBi. The type
TBI severity is attributed at the first moment from and degree of cognitive impairment following TBI may the Glasgow scale, coma and Post Traumatic Amnesia vary widely, depending on the severity and site of injury. period. A TBI is considered severe when the GCS is from If a focal brain injury occurs, the consequence may be 3 to 8, the period of coma is longer than 6 hours and the similar to the injury caused by a CVA, such as aphasia, PTA period is longer than 24 hours; in a moderate TBI apraxia, unilateral neglect or visuospatial dysfunction. the GCS is from 9 to 12, the period of coma shorter than However, these are the typical findings following TBI. 6 hours and the PTA from 1 to 24 hours; mild cases have Due to the mechanisms of acceleration-deceleration 270 BPSD and TBI Anghinah R, et al. Dement Neuropsychol 2013 September;7(3):269-277 that usually damage the ventral and lateral regions of dition to having to adjust to dysregulation in behavior, the frontal and temporal lobes, the most commonly emotions, thinking, and physical challenges, persons found sequelae are attention and memory deficit, dif- with TBI must make these adjustments with a brain ficulty learning new information, resolving problems, that processes information poorly. A person with lim- planning, as well as problems associated with impulsiv- ited coping skills may become frustrated with his or ity and self-control. Some “subclinical” findings such as her mood variability or with limb weakness, and may changes in naming, verbal fluency and auditory discrim- as a result have outbursts. Problems with attention, de- creased ability to understand, and difficulty remember- Initially, attention deficits are the most common and ing things may impact an individual’s ability to adjust severe in the residual stage, usually involving difficulty The patient may lose the information given at the The long-term memory is generally restored, but doctor’s office, or may forget to use the assistive device. some individuals continue having difficulties in learn- He or she may have problems perceiving situations or ing new things and retaining new information. Work- attribute incorrect motives to the actions of others.12 ing memory is frequently affected including the stages of encoding, storage and retrieval of information. Such BPSD - most common syndromes post-tBi. The most com-
changes exert a significant impact on social and voca- mon syndromes post-TBI are behavioral disinhibition, depression/anxiety/psychosis, substance abuse and at- Some individuals are left with amnesic syndrome, which is more common in those who have gone through Post-traumatic stress disorder (PTSD) occurs in up to 27% of cases, including patients with no clear recall of Executive functions may be affected, being related to the event. Depression has an incidence of 15% to 33% frontal lobe damage. When the frontal injury is severe and prevalence of 18% to 42%. Mania occurs in <10% the patient may be inert or lack initiative (medial or lat- of patients with TBI.8 Aggression occurs in variable fre- eral frontal injury), or display inappropriate and impul- quencies (ranging from 20% to 49%) and psychosis oc- sive behavior. Many individuals with frontal lobe injury in post-TBI retain much of their skills but are unable to initiate, sequence, organize or monitor their actions so noradrenergic medication. Noradrenergic agonists are used
as to meet the targets or goals set.
with varying degrees of success for the behavioral se- The language disorders most commonly observed quelae of brain injury, such as problems with attention, occur in the discursive (tendency to produce irrelevant impulsivity and speed of cognitive processing.13 information and omit important information), prag- Three commonly studied noradrenergic medications matic (loss in production of inferences, difficulty in for- are amphetamine, methylphenidate, and L-threo-3,4- mulating arguments) and conversation levels (loss of dihydroxyphenylserine (L-DOPS). Amphetamine en- initiative and maintenance of topics with inconsistent hances norepinephrine release from nerve terminals, switching without signaling). These changes correlate methylphenidate blocks the reuptake of NE, and L- with cognitive impairments in attention, memory and DOPS is a precursor of norepinephrine.14 A recent Co- chrane review concluded that there is insufficient evi- The inability to curb impulsive reactions leads to so- dence to support the routine use of methylphenidate or cial and family relationship problems. Patients usually have poor self-critical awareness regarding their condi-tion and behavioral changes.
Dopaminergic medication. Most dopaminergic cell bodies
reside in the substantia nigra or hypothalamus. Dopa-
long-term neuropsychiatric sequelae. Once patients have
mine appears to be important in memory, arousal, and survived the acute and subacute phases, many are left executive function. Medications that affect the dopami- with neuropsychiatric impairments. Common issues nergic system are used to treat disorders such as Parkin- related to symptoms include behavioral outbursts, son disease, attention deficit hyperactivity disorder, and emotional adjustments, cognitive deficits, and physical McDowell et al. (1998) used bromocriptine in a dou- The link between ability to adjust to TBI and the ca- ble-blind, placebo-controlled trial of 24 subjects who pacity to do so is complicated by a major factor. In ad- had suffered moderate to severe TBI at least 4 weeks Anghinah R, et al. BPSD and TBI 271 Dement Neuropsychol 2013 September;7(3):269-277 before treatment. The patients showed a significant im- fluid levels of ACh fluctuate after TBI, rising in the acute provement on several tasks thought to specifically rep- phase followed by a prolonged period of depression.26,27 Cholinergic circuits are vulnerable to injury.14 Schneider et al. (1999) found no difference in the Damage to the cholinergic basal forebrain septo- rate of cognitive recovery with amantadine treatment in hippocampal pathways results in severe depletions of a double-blind, placebo-controlled crossover trial of 10 ACh and has been associated with learning and memory subjects with moderate to severe TBI.18 A retrospective review by Passler et al. (2001) reported that patients In the study of Cardenas et al. (1994) – a blinded, given bromocriptine recovered faster from a vegetative controlled trial of 36 subjects after TBI – a significant number demonstrated improved memory and balance It is believed that dopamine has a role in brain injury rehabilitation, either as a primary effect or through its Donepezil, an anticholinergic medication used to treat Alzheimer disease and approved by the Food and Drug Administration (FDA), has been reported to im- Serotonergic medication. Serotonin has behavioral effects
prove memory problems after TBI, at least during the and is involved in motor control.20 The study of Lou- binoux et al. (2002) found that a single dose of parox- More research is needed to better define the role of etine increased functional MRI (fMRI) motor cortex activation in human subjects during a simple motor paradigm.21 Another serotonin reuptake inhibitor, flu- voxamine, has been shown to improve reaction time.22,23 Subjects. This was a retrospective study of fifteen pa-
Serotonergic drugs have not been shown to be effec- tients with a diagnosis of traumatic brain injury fol- tive in reducing symptoms after brain injury in human lowed at the Outpatient Clinic of the Clinicas Hospital In severe TBI, BAY x 3702 was administered in a mul- ticenter, randomized double-blind, placebo-controlled Strategies to manage post-tBi patients. Cognitive function
parallel group study. BAY x 3702 was found to be safe, evaluation – The patient will initially be subjected to a but the effect on outcome was not significant.24 reading test, which consists of reading simple children’s Serotonergic medications are often prescribed to pa- books allowing evaluation of how long they focus on tients recovering from TBI because of the relative safety the book. According to the performance and education of, and their role in, treating disorders of mood and be- of each individual, slightly more complex texts will be havior. Data from animal and human studies suggest that these drugs are safe when given during rehabilita- After this first test, each patient will be classified ac- tion after traumatic or ischemic brain injury. It is still cording to the Rancho Los Amigos scale and only those unclear if serotonergic medication has only immediate who score greater than or equal to 5 (on a scale of 8) will effects on behavior or whether they have a long-lasting be referred for cognitive rehabilitation.33 This is necessary because, in order to be rehabilitat- ed, the individual must maintain a minimum time set in cholinergic system. Acetylcholine is produced in sev-
eral nuclei of the brain including the nucleus basalis of The next intervention will be to conduct a neuropsy- Meynert and several tegmental nuclei, with widespread chological evaluation, speech and occupational therapy projections to the cerebral cortex, hippocampus, amyg- including the Mini-Mental State Examination34,35 and dala, hypothalamus, cingulum, and thalamus.25 Acetyl- clock drawing test. The neuropsychological assessment choline (Ach) can act as a neuromodulator and change includes the evaluation of affective/emotional state the magnitude of other synaptic events. ACh was the (BECK scale – BDI, BAI, BHS, BSI),36 I.S.S.L37 and GDS,38 first neurotransmitter targeted to improve recovery af- activities of daily living PFEFFER,39 batteries of tests of executive functions Wisconsin,40 Stroop (Stroop In- Acetylcholine is involved in memory and recently terference Test – Victoria version) - freely translated the use of cholinergic drugs in Alzheimer disease was from the English version.41,42 The Rey complex Figure,43 approved. There is growing evidence of the role of ACh WAIS-III,44 attention,44 the Wechsler Digit Symbol-Cod- in experience-driven cortical plasticity.14 Cerebrospinal ing, trail making parts A and B (Trail Making Test),45 272 BPSD and TBI Anghinah R, et al. Dement Neuropsychol 2013 September;7(3):269-277 visuo-constructive,44 language FAS and Verbal Fluen- problems and iatrogenic contributions; and [3] imple- cy,46 memory,44 and Rey Auditory-Verbal Learning Test mentation of nonpharmacological treatment.
(RAVLT)43,47 will also be applied. All tests have been vali- The initial steps of treatment include a comprehen- dated for use in Brazil with scores for different levels of sive neuropsychiatric evaluation and testing. This may entail neurological and psychiatric examination to doc- The speech evaluation includes pragmatic assess- ument baseline deficits, diagnoses, and functioning.
ment, according to precepts of conversational analysis, A neuropsychological battery documents the cogni- a test of verbal working memory for auditory input tive skills and limitations, and provides a baseline from (N-Back) language evaluation, the Arizona Battery for which gains in cognitive rehabilitation can be bench- marked. Neurophysiological tests may show brain dys- The tests applied have been validated for use in Bra- function and seizures. When indicated, neuroimaging zil with scores according to different levels of schooling may be of benefit to show ischemia, hemorrhage, en- except for the “Test of Practical Judgment” (TOP-J), cephalomalacia, neuronal loss, and altered cerebral me- which does not have a version in Portuguese and the Arizona Battery for Communication Disorders – ABCD, The pharmacological approach focuses on functional which is undergoing the validation process, and will recovery and its target of therapy is symptom reduction be included in our battery. Computerized tests that through pharmacological enhancement of rehabilita- evaluate response time for a particular task will also be tion. Most drugs affect more than one neurotransmitter systems, in various parts of the nervous system. After a Occupational therapy evaluates cognition in order to TBI, neurotransmitter levels change and may be a target determine the individual’s capacity to live alone safely of therapy. Glutamate and aspartate are released exces- and comfortably, to work or undertake any activity they sively, cortical levels of dopamine are suppressed for at deem important or meaningful49. Also, it limits the least several weeks after TBI. The levels of norepineph- impact of deficits in memory, attention and executive rine and acetylcholine fluctuate, with an initial increase functions in performing the activities of daily living. The evaluation of performance in BADL and IADL requires After the evaluations, rehabilitation strategies will the observation of the individual’s behavior in the con- be developed, in conjunction with the interdisciplinary text in which they conduct these activities. The infor- team, for each patient individually. And if necessary, the mation obtained will be used to develop strategies, with pharmacological approach will be adopted.
the individual and their family, which will minimize the losses in each cognitive deficit.
Through the evaluation of cognitive abilities in the Our experience using the Pharmacological TBI Guide- tasks, it is possible to determine the patient’s strengths, line approach for 15 outpatients with BPSD showed that limitations and challenges in learning abilities and en- the patients improved with the use of mood stabilizers, vironmental strategies that will support their daily selective serotonin reuptake inhibitors and dopamine- life.50,51 Assessment in Occupational Therapy includes stimulating drugs. The causes of TBI and the drugs in use among the TBI patients are shown in Table 1.
After the neuropsychological, speech and occupa- tional therapy evaluation, rehabilitation strategies will DiScuSSion
be developed, together with the interdisciplinary team, Valproic acid – a mood stabilizer – and venlafaxine – a drug that has dual action with selective serotonin reup-take inhibitors (SSRI) and adrenergic reuptake, in addi- Pharmacological treatment approach– Brain injury con- tion to weak action as a dopamine stimulant – are the fers increased sensitivity to the active agents of the cen- two medications with the best indication for TBI in our tral nervous system (CNS); therefore, treatment and side milieu, where possible replacing with hidantal (phenyt- effects may be accentuated at lower doses in patients oin) or gardenal (phenobarbital) when the patient uses neuroleptics. An anticholinesterase inhibitor, originally Secondly, to systematically approach treatment in developed for Alzheimer’s disease, is used for improving TBI beyond pharmacological interventions, three areas are important to bear in mind: [1] identification of tar- Amantadine – a weak antagonist of the NMDA type get symptoms; [2] consideration of coexisting medical glutamate receptor, that increases dopamine release Anghinah R, et al. BPSD and TBI 273 Dement Neuropsychol 2013 September;7(3):269-277 table 1. Profile of TBI patients.
causes of tBi
medication in use
and blocks dopamine reuptake – is a good option for threshold. Low histamine, cholinergic, and a-adrenergic enhancing attention. It has been used for Parkinson’s binding SSRIs are preferred for mood and anxiety, but Disease. Modafinil was used to treat hypersomnia.
side effects of sexual dysfunction, dyspepsia, drowsi-ness, and irritability may limit their use in TBI. A few motivation. Lack of motivation is very common after a
studies have shown that stimulants, amantadine, and significant head injury. Injuries to the orbitofrontal, anticholinesterase drugs are helpful.57-59 The drugs of medial frontal cortical, ventral pallidum and ventral choice for post-traumatic mania are clonidine, carba- tegmentum may all affect motivation.54 A poverty of be- mazepine, and divalproex. Lithium is reserved for pa- havior and speech, lack of initiative, loss of emotional responses, and severe psychomotor problems can be classified as a more extreme form of abulia. Both phar- Psychotic disorders. The onset of psychotic symptoms is
macological treatment and behavioral interventions usually delayed following the injury, by around 4 years.61 are necessary to treat these syndromes. Stimulants and The psychoses are characterized by hallucinations and dopaminergic medications, as well as activating antide- pressants such as bupropion or monoamine oxidase in- TBI psychosis differs from schizophrenia because hibitors (MAOIs) are good options. Selective serotonin of the absence of Schneiderian first-rank symptoms in reuptake inhibitors (SSRIs) and typical neuroleptics are non-delirium associated hallucinations that can occur bad choices, worsening these syndromes.55 post-TBI. A later age of onset, less premorbid psychi-atric disturbance, briefer duration, less common fam- mood disorders. Following TBI, up to 50% of patients have
ily history, better response to neuroleptics, less need symptoms of depression, with 20% meeting Diagnostic for maintenance medication, and a better prognosis and Statistical Manual of Mental Disorders, Fourth Edi- are other factors distinguishing TBI psychosis from tion (DSM-IV) criteria for major depression. These pa- tients have a significantly increased risk of suicide.12 Neuroleptics may cause adverse reactions, so it is im- Tricyclic antidepressants (TCAs) may be a good op- portant to initiate the treatment for post-TBI psychosis tion to treat anxiety and depression56 but they should at one third to one half the usual doses.63 Neuroleptics be limited to agents with the least anticholinergic activ- may impede cognitive recovery.64 Atypical neuroleptics, ity, the least sedation, and the least effect on the seizure except for clozapine (which is an anticholinergic and 274 BPSD and TBI Anghinah R, et al. Dement Neuropsychol 2013 September;7(3):269-277 lowers the seizure threshold) are the drugs of choice. is very common to find explosive personality disorders, Benzodiazepines should be used sparingly.12 particularly among patients who use alcohol. Counseling is necessary for treatment of these various personality Post-traumatic stress disorder and other anxiety disorders.
changes. The use of tricyclic and SSRI antidepressants Anxiety can occur in patients who have suffered a TBI, may help with lability. Some studies have demonstrated presenting as insomnia, inability to concentrate, free- that impulsivity can be controlled with low-dose stimu- floating phobias, and panic attacks. Situations in which the patients know that they cannot perform as well as they did before their TBI cause anxiety. It is important Aggressive disorders. In the delirious subacute phase of
that the patient understands the injury and learns how recovery, agitation occurs frequently. Aggression in pa- to deal with his/her limitations. In an acute stress situ- tients with TBI is generally reactive without premedi- ation, a short course of a short-acting benzodiazepine tation, and is nonpurposeful, explosive, periodic, and may help. Selective serotonin reuptake inhibitors (SS- RIs) may be helpful but they should be used with care The aggressive behavior is associated with damage to because they can exacerbate apathy and cause sexual the limbic system, orbitofrontal cortex, left anterome- dysfunction. Antiepileptic drugs (AEDs) may also be dial frontal lobe, and anterior cingulate.69 useful, particularly in patients who are aggressive.12 Many of the agents used for agitation are also used for aggression. Antipsychotic medications do not help with Somatoform disorders. Somatization may manifest as
chronic, nonpsychotic aggression. Akathisia is a com- dizziness, vertigo, gait instability, headache, fatigue, mon adverse reaction to typical neuroleptics and may malaise, tinnitus, visual disturbances, cognitive ‘‘fog- increase violent behavior. It has been demonstrated that giness,’’ nonneuroanatomical paresthesias, weakness, neuroleptics are responsible for slow recovery from TBI.12 focal deficits, and nonepileptic events.12 Patients pre- Benzodiazepines and low-dose buspirone may cause senting these symptoms are often classified as having a paradoxical reaction. Antipsychotic agents should be ‘‘postconcussional syndrome”.65 Cognitive behavior used for patients who are indeed psychotic. The use therapy (CBT) may be useful for non-TBI populations of carbamazepine, valproic acid, gabapentin and ox- but treatment for these disorders are lacking.12 carbazepine has proven successful in some patients. Lithium is a good option in patients who are manic or cognitive disorders. These disorders are among the most
that display cyclic violence. High-dose propranolol has commonly occurring sequelae in TBI and post-traumatic proven very helpful in some patients. Antidepressant cholinergic deficits are thought to contribute to the de- medications, such as TCAs and SSRIs, have been shown velopment of post-traumatic cognitive impairments.12 The study of Silver et al. (2006) – a randomized double- In conclusion, traumatic brain injury can cause a blind placebo-controlled study of a cholinesterase in- variety of potentially disabling psychiatric symptoms hibitor in 157 post-TBI patients – showed no difference and syndromes. These include mood and anxiety disor- from placebo in both primary cognitive and secondary ders; personality disturbances; aggression; and, often, psychosis. The diagnosis of cognitive and behavioral disorders following TBI can be complex. It is therefore Personality change due to medical condition. The personal-
essential that the physician obtain a broad picture of ity changes are most often exaggerations of premorbid the patient before prescribing medications. A differen- personality traits and may include lability, disinhibition, tial diagnostic approach can help the physician to sort aggression, apathy, and paranoia. Impulsivity, lack of through the numerous etiological factors that may be empathy, loss of a sense of self, and inability to moni- contributing to the patient’s condition. Pharmacologi- tor one’s own behavior are typical of the ‘‘pseudoborder- cal treatment may include a wide range of medications, line’’ personality disorder. Damage to the orbitofrontal such as antidepressants, antipsychotics, mood stabiliz- cortex may cause mania, euphoria, and impulsivity that ers, and stimulants. Family and individual counseling are labeled as ‘‘pseudosociopathic syndrome’ . A ‘‘pseu- is particularly important in helping the patient and the dodepressed’’ personality disorder can be the result of family reconcile themselves to the reality of the behav- medial frontal damage and may cause severe apathy. It ioral changes in the patient post-TBI.
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