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[WEB SITE] Traumatic Brain Injury Rehabilitation at Florida Institute for Neurologic Rehabilitation

A Specialized Approach to NeuroRehabilitation & Traumatic Brain Injury Rehabilitation

The Florida Institute for Neurologic Rehabilitation, (FINR) has developed a comprehensive brain injury rehabilitation continuum of care offering specialized inpatient evaluation and treatment for both children and adults. Through a pre-admission evaluation and medical records review, FINR develops individualized treatment programs. As a leader in traumatic brain injury rehabilitation (TBI)neurorehabilitation, and neuropsychiatric disorders, our continuum of care delivers clinically relevant and cost effective services with unparalleled continuity of care. The distinct programs in our continuum are designed for individuals with a wide range of complex medical, neurorehabilitation, neurobehavioral, and neuropsychiatric care needs.

Potential traumatic brain injury rehabilitation clients, family members, funders, referral sources, and other concerned parties are encouraged to tour our facilities in order to make informed placement decisions. If our team of expert staff can assist in scheduling a tour or providing educational resources and information, please give us a call at 1-888-TBI-FINR (888-824-3467).

 

 

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[ARTICLE] Pharmacological interventions for traumatic brain injury – Full Text 

Psychostimulants, antidepressants, and other agents may speed the recovery of patients suffering from the functional deficits that follow an insult to the brain.

Traumatic brain injury is common in North America and has dramatic and wide-ranging effects on survivors’ quality of life. Those who survive traumatic brain injury may experience anxiety, agitation, memory impairments, and behavioral changes. When managing the immediate and long-term consequences of such injuries, clinicians have many pharmacological options, including psychostimulants, antidepressants, antiparkinsonian agents, and anticonvulsants. These and other agents can play a role in managing the neuropsychiatric, neurocognitive, and neurobehavioral sequelae of injury to the brain.

Traumatic brain injury (TBI) is commonly defined as an insult to the brain from an external force that causes temporary or permanent impairment in functional, psychosocial, or physical abilities.1 It is a significant cause of morbidity and mortality, and the leading cause of death and disability among young adults.

Common causes of TBI include motor vehicle accidents, falls, sports injuries, and violence,[1] and it is recog­nized increasingly in war zone injury.[2] In the US, approximately 2 million people will sustain a TBI each year, one-quarter of whom will require hospitalization, leading to a conservative estimate of direct and indirect costs of $50 billion to $100 billion annually.[3]

With advances in the management of head trauma, an increasing number of patients are surviving with residual neurological impairments. A National Institute of Health panel estimates that 2.5 to 6.5 million Americans currently live with TBI-related disabilities.[4]

The effective treatment of TBI requires input from multiple disciplines and professions starting at the time of injury and continuing through the rehabilitation phase.

Despite the prevalence and cost of TBI-related disabilities there is a paucity of literature reviewing modern approaches to pharmacotherapy. There is, however, growing evidence that medications may speed recovery by enhancing some neurological functions without impact­ing others.

Pharmacotherapy is in­creasingly being used in both the subacute (less than 1 month post-TBI) and chronic (more than 1 month post-TBI) phases.

Disabilities arising from TBI that have a direct impact on functioning and rehabilitative potential can be broadly classified into four main categories: decreased level of consciousness (LOC), and neuropsychiatric, neurocognitive, and neurobehavioral sequelae.5-8 Decreased level of consciousness refers to a diverse range of clinical states including coma, vegetative states, akinetic mutism, and locked-in states.

Neuropsychiatric symp­toms may present as mood disorders, posttraumatic stress disorder, and personality changes characterized by disinhibition and egocentricity. Neurocognitive injuries vary, but most frequently involve impaired attention, memory, and executive functioning.

Neurobehavioral deficits distinct from neuropsychiatric sequelae may take the form of irritability, hyperexcitability, nervousness, disinhibition, poor impulse control, restlessness, and aggression, with aggression and agitation seen in as many as 30% of brain-injured patients.[5-8]

Depending on the location of in­jury, damage can occur to a variety of neurotransmitter networks critical to cognitive processes. Investigation has focused on the loss of dopaminergic neurons that regulate executive functioning, as well as deficits in norepinephrine and acetylcholine, which limit attention—a critical function for effective rehabilitation.[9]

Fortunately, a number of pharmacological interventions show promise in helping patients cope with these losses and deficits.

Although insufficient evidence exists to establish guidelines for optimal pharmocotherapy, medications may be used to support recovery. Examples are shown in the accompanying Table, which summarizes the pharmacological approaches discussed in more detail below.

When problematic TBI symptoms are identified, clinicians can use this information to determine pharmacological options and integrate them with nonpharmacological options such as physical therapy, occupational therapy, physiatry, and the patient’s support network.

Planning a pharmacological intervention strategy
The decision to use pharmacological intervention should be the result of multidisciplinary collaboration and made with the patient or his or her substitute decision maker. Goals of therapy should be clarified, and outcomes and adverse events should be reliably tracked, particularly so medications that are ineffective or cause adverse events can be discontinued and unnecessary polypharmacy can be avoided.

Selecting the most appropriate agent requires careful analysis of the neurological disabilities present, the nature of the underlying lesion, and the time elapsed since the injury.

Psychostimulants
Psychostimulants such as methylpheni­date are most commonly used to treat attention deficit hyperactivity disorder (ADHD), a condition that involves problems with executive functioning and can be characterized as similar to brain injury both in terms of symptoms and neurotransmitter aberrations.[10]

Although the complete mechanism of action of methylphenidate remains unknown, this agent is thought to bind dopamine transporters, thereby blocking reuptake and increasing extracellular dopamine levels, particularly in the frontal cortex.[11] It is also thought to increase norepinephrine and serotonin levels.

In the majority of studies, methylphenidate has been administered  twice daily, either at a fixed dose of 10 to 15 mg or at a dose of 0.3 mg/kg.[12-15]

In the acute phase after a TBI, methylphenidate-treated patients dem­onstrated better attention, concentration, and performance on motor memory tasks at 1 month, but these benefits did not persist at 3 months. Thus, it has been suggested that while methyl­phenidate may shorten recovery time, it does not change morbidity.[12]

In the chronic phase after a TBI, patients have reported improvements in mood, work performance, and alertness, with more limited evidence suggesting an improvement of fluency and selective attention.

The impact of methylphenidate on chronic attention is more ambiguous: one study suggests improvement in long-term processing speed and attention to tasks but not increased sustained attention or decreased susceptibility to distraction.[12]

Two separate studies have suggested methylphenidate is effective in the treatment of agitation and sei­zures,[16,17] while another demonstrated no neurobehavioral benefit.[18]

Despite the accumulation of controlled clinical trials, there is no consensus on the use of stimulants in treating TBI-induced impairments in arousal and motor activity.

It should be noted that one recent review concluded “at present there is insufficient evidence to support routine use of methylphenidate or other amphetamines to promote recovery from TBI,”[19] while another review noted that at least 10 clinical trials have demonstrated a role for methylpheni­date in both adult and pediatric brain injury patients suffering from neurocognitive deficits, particularly in attention, memory, cognitive processing, and speech.[20]

Methylphenidate has a quick onset of action and relatively benign side effect profile, and we believe it to be useful in both the acute and chronic phase of TBI.

Antidepressants
Despite potentially severe consequenc­es, post-TBI psychiatric sequelae are underdiagnosed and undertreated. Fortunately, current evidence suggests that antidepressants can be used to manage both neuropsychiatric and additional neurological deficits persisting from brain injury.

Selective serotonin reuptake inhi­bitors (SSRIs) have been found useful in treating behavioral syndromes in TBI patients, particularly in the subacute stages of recovery[21] but also in chronic settings.

The majority of studies suggest that SSRIs improve neurobehavioral, neurocognitive, and neuropsychiatric deficits, specifically agitation, depression, psychomotor retardation, and recent memory loss; however, most data originates from nonrandomized trials.

Sertraline administered at an average dose of 100 mg daily for 8 weeks has been found to be beneficial for agitation, depressed mood, and deficits in psychomotor speed and recent memory; shorter treatment durations have demonstrated no benefit.[21]

Similarly, 60 mg daily of fluoxetine for 3 months was shown to be effective in the treatment of obsessive-compulsive disorder caused by brain injury.[22] Finally, paroxetine or citalopram, at a dose of 10 to 40 mg daily, was shown by another study to be equally effective in the treatment of pathological crying.[23] None of the re­viewed studies addressed neurocognitive deficits.

The highest concentration of serotonergic and adrenergic fibres is located near the frontal lobes, the most common site of traumatic contusion.[24]

Consequently, these fibres are commonly injured in TBI, suggesting that newer antidepressants with effects on both norepinephrine and serotonin, such as mirtazapine and venlafaxine, may also be effective in the treatment of TBI sequelae; however, clinical data with these agents in TBI is lacking.

Similarly, bupropion increases both dopamine and norepinephrine levels and is a weak inhibitor of serotonin reuptake. At 150 mg daily, this agent has been useful in treating restlessness.[25]

Antiparkinsonian drugs
The antiparkinsonian drugs amantadine, bromocriptine, and levodopa combined with carbidopa (e.g., Sine­met) have varied mechanisms of action, but all ultimately serve to increase dopamine levels in the brain.

Amantadine acts presynaptically to enhance dopamine release or inhibit its reuptake, and can act postsynaptically to increase the number, or alter the configuration of, dopamine re­ceptors.[26] It is also a noncompetitive NMDA receptor antagonist and may provide protection against possible glutamate-mediated excitotoxicity in the context of TBI.[27]

Bromocriptine is a dopamine receptor agonist affecting primarily D2 receptors and to a lesser extent D1 receptors.[28] The use of levodopa and carbidopa in combination directly increases dopamine levels: levodopa becomes dopamine once de­carboxylated, while carbidopa inhibits L-amino decarboxylase, allowing levodopa to reach the central nervous system.[28]

Multiple studies of amantadine at a dose of 100 to 300 mg daily have suggested its effectiveness in both the acute and chronic care phases after TBI, particularly in diffuse, frontal, or right-sided brain injury.

Currently, the evidence suggests neurocognitive or neurobehavioral deficits, particularly cognition difficulties and agitation, are primary indications for amantadine use.[26,29,30]

Amantadine-treated patients demonstrated improvements in motivation; decreased level of apathy; increased attention, concentration, and alertness; improved executive functioning; decreased processing time; reduced agitation, distractibility, fatigue, aggression, and anxiety.

In addition, patients treated with amantadine demonstrated changes in outcome LOC, specifically improved arousal and LOC as measured by the Glasgow Coma Scale. Interestingly, one study also suggested decreased mortality.[31] To date, no study has shown an improvement in memory.

Three case reports using 5 to 45 mg of bromocriptine daily,[32] and one study using a combination of 100 mg of bromocriptine with 100 mg of ephedrine,[33] showed improvement in akinetic mutism, while another study using 5 mg of bromocriptine combined with sensory stimulation led to improvements in patients with vegetative or minimal consciousness.[34]

The evidence is similarly limited for levidopa and carbidopa medications where nonrandomized studies suggest that they might be useful in the chronic phase of TBI with diffuse injury and persistent vegetative state.[35]

Combining agents has also been tried in one study that found improvements in neuropsychiatric deficits with the daily administration of 25 mg/200 mg of levodopa/carbidopa three times daily, 250 mg of amantadine, and 5 mg of bromocriptine twice daily.[36]

Anticonvulsants
Anticonvulsants have been used with varying results for treating symptoms of TBI. Valproic acid, for example, enhances inhibitory control mediated by the neurotransmitter GABA, thereby promoting general central nervous system stabilization, but findings thus far have been mixed.

Investigations utilizing 600 to 2250 mg of valproic acid daily (resulting in serum levels of 40 to 100 µg/mL), have demonstrated positive neurocognitive effects, in­cluding improved recent memory and problem-solving, as well as ameliorating neuropsychiatric and neuro­behavioral symptoms such as depression, mania, destructive and aggressive behavior, restlessness, disinhibition, impulsivity, lability, and alertness.[37-41]

Conversely, one control­led trial found valproic acid negatively impacted decision-making speed, and another suggested an increased mortality rate with valproic acid use.[37-41]

Other agents
Modafinil is a vigilance-promoting drug commonly used to treat narcolepsy and idiopathic hypersomnia, illnesses that can present with symptoms similar to those seen in TBI: excessive daytime sleepiness, inattention, and decreased ability to perform social activities.

The precise mechanism of action remains unknown, although it is believed that modafinil can inhibit GABA or increase glutamate levels in the nondopaminergic anterior hypothalamus, hippocampus, and amygdale.[42,43]

Two studies that investigated the role of modafinil in chronic TBI showed an improvement in neurocognitive deficits, specifically memory and attention, as well as improving daytime somnolence at doses between 100 and 400 mg.[44,45]

Four randomized control trials examining the use of beta-blockers, specifically propranolol and pindolol, have demonstrated beneficial effects on neurobehavioral symptoms of ag­gression and agitation in both the chronic and subacute phase. This class of drugs deserves further attention for the management of both neuropsychiatric and neurobehavioral sequelae of TBI.[46]

Neuroleptics are being used in­creasingly in the setting of delirium, and one might consider using them in an attempt to allow the brain to recalibrate neurotransmitter levels. However, it should be noted that there is some evidence that dopamine blockade may negatively affect recovery.[47,48]

There are also a number of animal studies examining drugs that have the potential to adversely affect brain recovery following TBI. These studies typically use a stroke model, so generalizing to TBI may not be possible.

Nevertheless, the evidence currently does not support the use of neuro­leptics, benzodiazepines, phen­y­toin, prazosin, trazodone, and similar agents because of their potential adverse effect on recovery, presumably through the impacts they have on neurotransmitters such as dopamine, norepinephrine, or GABA.[49-51]

Preliminary evidence suggests cho­linesterase inhibitors such as don­epezil may improve long-term cognitive outcomes, particularly in domains such as memory and attention when administered early, and further in­vestigation with these agents is also warranted.[52,53]

Finally, antiandrogenic medications, such as estrogen and medroxyprogesterone, may have a role to play in reducing inappropriate sexual be­havior in patients with TBI. In a case study and one small trial, these drugs demonstrated effectiveness.[54]

Summary
The nature of TBI sequelae, whether psychiatric, cognitive, or behavioral, is poorly understood. Likewise, the use of pharmacological interventions to improve symptoms, function, and outcome is still under development.

There are, however, a number of agents that inspire optimism. When treating neurological deficits medically, there is evidence to support the tailored use of these agents for particular TBI clinical scenarios. The timing and nature of symptoms, along with wheth­er agents are administered in the acute or chronic phase after TBI, are all relevant factors for determining proper use.

With insufficient evidence to establish guidelines for optimal treatment, care must be taken when choosing pharmacological interventions for TBI.

If the decision is made to use medications to promote TBI recovery or treat its attendant disabilities, clinicians should thoroughly document the goals of pharmacotherapy and closely monitor for side effects. Future studies will undoubtedly add to the clinician’s armamentarium for the care of TBI patients.

Competing interests
None declared.


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Source: Pharmacological interventions for traumatic brain injury | BC Medical Journal

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[ARTICLE] Notes on Human Trials of Transcranial Direct Current Stimulation between 1960 and 1998 – Full Text

Background: Transcranial direct current stimulation (tDCS) is investigated to modulate neuronal function including cognitive neuroscience and neuropsychiatric therapies. While cases of human stimulation with rudimentary batteries date back more than 200 years, clinical trials with current controlled stimulation were published intermittently since the 1960s. The modern era of tDCS only started after 1998.

Objectives: To review methods and outcomes of tDCS studies from old literature (between 1960 and 1998) with intention of providing new insight for ongoing tDCS trials and development of tDCS protocols especially for the purpose of treatment.

Methods: Articles were identified through a search in PubMed and through the reference list from its selected articles. We included only non-invasive human studies that provided controlled direct current and were written in English, French, Spanish or Portuguese before the year of 1998, the date in which modern stimulation paradigms were implemented.

Results: Fifteen articles met our criteria. The majority were small-randomized controlled clinical trials that enrolled a mean of approximately 26 subjects (Phase II studies). Most of the studies (around 83%) assessed the role of tDCS in the treatment of psychiatric conditions, in which the main outcomes were measured by means of behavioral scales and clinical observation, but the diagnostic precision and the quality of outcome monitoring, including adverse events, were deficient by modern standards. Compared to modern tDCS dose, the stimulation intensities used (0.1–1 mA) were lower, however as the electrodes were typically smaller (e.g., 1.26 cm2), the average electrode current density (0.2 mA/cm2) was approximately 4× higher. The number of sessions ranged from one to 120 (median 14). Notably, the stimulation session durations of several minutes to 11 h (median 4.5 h) could markedly exceed modern tDCS protocols. Twelve studies out of 15 showed positive results. Only mild side effects were reported, with headache and skin alterations the most common.

Conclusion: Most of the studies identified were for psychiatric indications, especially in patients with depression and/or schizophrenia and majority indicated some positive results. Variability in outcome is noted across trials and within trials across subjects, but overall results were reported as encouraging, and consistent with modern efforts, given some responders and mild side effects. The significant difference with modern dose, low current with smaller electrode size and interestingly much longer stimulation duration may worth considering.

Introduction

Transcranial direct current stimulation (tDCS) consists of applying a weak direct current on the scalp, a portion of which crosses the skull (Datta et al., 2009) and induces cortical changes (Fregni and Pascual-Leone, 2007; Nitsche et al., 2008). The investigation of the application of electricity over the brain dates back to at least 200 years, when Giovanni Aldini (Zaghi et al., 2010) recommended galvanism for patients with deafness, amaurosis and “insanity”, reporting good results with this technique especially when used in patients with “melancholia”. Aldini also used tDCS in patients with symptoms of personality disorders and supposedly reported complete rehabilitation following transcranial administration of electric current (Parent, 2004).

These earliest studies used rudimentary batteries and so were constant voltage, where the resulting current depends on a variable body resistance. Over the 20th century, direct voltage continued to be used but most testing involved pulsed stimulation, starting with basic devices where a mechanical circuit that intermittently connected and broke the circuit between the battery and the subject and evolving to modern current control circuits including Cranial Electrotherapy Stimulation and its variants (Guleyupoglu et al., 2013). Interest in direct current stimulation (or tDCS) resurged with the studies of Priori et al. (1998) and Nitsche and Paulus (2000) that demonstrated weak direct current could change cortical response to Transcranial Magnetic Stimulation, thereby indicating that tDCS could change cortical “excitability”. Testing for clinical and cognitive modification soon followed (Fregni et al., 2005, 2006). Developments and challenges in tDCS research, including applications in the treatment of neuro-psychiatrics disease since 1998 have been reviewed in detailed elsewhere (Brunoni et al., 2012).

This historical note aims to explore earlier data on human trial using current controlled stimulation (tDCS) before 1998 with the goal of informing ongoing understanding and development of tDCS protocols. As expected, we found variability in the quality of trial design, data collection and reporting in these earlier studies. Nonetheless, many clinical findings are broadly consistent with modern efforts, including some encouraging results but also variability across subjects. We also describe a significant difference in dose with lower current, smaller electrodes and much longer durations (up to 11 h) than used in modern tDCS.

Figure 2. Summary of study parameters on human trials using transcranial direct current stimulation (tDCS) in old literature (from 1960 to 1998). Models of commonly used montages of tDCS in early studies (A); red: anode electrode(s), blue: cathode electrode(s). Total number of subjects in each group of patients participating in studies using aforementioned montages (B.1) and leading countries conducting tDCS studies in early stage with number of published articles (B.2).

Continue —> Frontiers | Notes on Human Trials of Transcranial Direct Current Stimulation between 1960 and 1998 | Frontiers in Human Neuroscience

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[ARTICLE] Exercise as medicine – evidence for prescribing exercise as therapy in 26 different chronic diseases – Full Text HTML/PDF

Abstract

Scandinavian Journal of Medicine & Science in SportsThis review provides the reader with the up-to-date evidence-based basis for prescribing exercise as medicine in the treatment of 26 different diseases: psychiatric diseases (depression, anxiety, stress, schizophrenia); neurological diseases (dementia, Parkinson’s disease, multiple sclerosis); metabolic diseases (obesity, hyperlipidemia, metabolic syndrome, polycystic ovarian syndrome, type 2 diabetes, type 1 diabetes); cardiovascular diseases (hypertension, coronary heart disease, heart failure, cerebral apoplexy, and claudication intermittent); pulmonary diseases (chronic obstructive pulmonary disease, asthma, cystic fibrosis); musculo-skeletal disorders (osteoarthritis, osteoporosis, back pain, rheumatoid arthritis); and cancer. The effect of exercise therapy on disease pathogenesis and symptoms are given and the possible mechanisms of action are discussed. We have interpreted the scientific literature and for each disease, we provide the reader with our best advice regarding the optimal type and dose for prescription of exercise.

Introduction

Here we present an update of a previously published review “Evidence for prescribing exercise as therapy in chronic disease” from 2006 (Pedersen & Saltin, 2006). Physical activity represents a cornerstone in the primary prevention of at least 35 chronic conditions (Booth et al., 2012). However, over the past two decades, considerable knowledge has accumulated concerning the significance of exercise as the first-line treatment of several chronic diseases. Of note, today exercise has a role as medicine in diseases that do not primarily manifest as disorders of the locomotive apparatus. When we selected diagnoses to be included in this review, we took into account both the frequency of the diseases and the relative need for exercise therapy. Twenty-six diseases covering various aspects of the medical curriculum are included. These are psychiatric diseases (depression, anxiety, stress, schizophrenia); neurological diseases (dementia, Parkinson’s disease, multiple sclerosis); metabolic diseases (adiposity, hyperlipidemia, metabolic syndrome, polycystic ovarian syndrome, type 2 diabetes, type 1 diabetes); cardiovascular diseases (hypertension, coronary heart disease, heart failure, cerebral apoplexy, and intermittent claudication); pulmonary diseases (chronic obstructive pulmonary disease, asthma, cystic fibrosis); musculo-skeletal disorders (osteoarthritis, osteoporosis, back pain, rheumatoid arthritis); and cancer. We provide the reader with the evidence-based basis for prescribing exercise as medicine for all of these diseases. We than briefly discuss possible mechanisms of action. Finally, regarding type and dose of exercise we suggest specific recommendations, which are based on evidence, experience and common sense.

Methods

A comprehensive literature search was carried out for each diagnosis in the Cochrane Library and MEDLINE databases (search terms: exercise therapy, training, physical fitness, physical activity, rehabilitation and aerobic). In addition, we sought literature by examining reference lists in original articles and reviews. We have primarily identified systematic reviews and meta-analyses and thereafter identified additional controlled trials. We then selected studies in which the intervention was aerobic or strength exercise and have given priority to randomized controlled trials (RCTs).

Continue —> Exercise as medicine – evidence for prescribing exercise as therapy in 26 different chronic diseases – Pedersen – 2015 – Scandinavian Journal of Medicine & Science in Sports – Wiley Online Library

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[WEB SITE] Neuropsychiatric Effects of Traumatic Brain Injury

From time to time every psychiatrist comes across patients whose problems are at least in part related to the neuropsychiatric consequences (behavioral, cognitive, and emotional) of traumatic brain injury (TBI). TBI affects approximately 2 of every 1000 persons per year. Those who are vulnerable to mental illness (eg, persons with alcohol abuse or antisocial personality disorder) are particularly at risk. Patients with TBI often have poor insight and may need hospitalization for their own safety. The neuropsychiatric and other sequelae are long-term; a head injury is for life.

A telling illustration from 1937 by Courville, a neuropathologist, nicely demonstrates why TBI is of interest to psychiatrists (see figure 1 in Fleminger 20091). The illustration is a composite of the location of contusions found in 50 patients who died of TBI.
The sites of specific vulnerability to contusions are the medial orbital frontal lobe and the anterior temporal lobes (Figure 1). Areas where contusions rarely occur include the primary motor, somato-sensory, and visual cortex. Therefore, areas of the brain concerned with social function and decision making are particularly vulnerable. It is unsurprising that neuropsychiatric sequelae outstrip neurophysical sequelae as the major cause of disability after TBI.

The neuropathology of TBI

Contusions are areas of cerebral bruising particularly involving gray matter, whereby blood leaks into the extravascular space. The contusion results in cell death and local loss of tissue. Diffuse axonal injury affects white matter anywhere throughout the cerebrum and brain stem. It may be followed by generalized atrophy with ventricular enlargement (Figure 2); this may take a few weeks or months to develop. Diffuse axonal injury in the brain stem is usually responsible for the slurred speech and severe ataxia that are seen in some severely disabled patients after TBI. Contusions and diffuse axonal injury may be complicated by anoxic brain injury that may occur soon after trauma because of poor cerebral perfusion secondary to raised intracranial pressure and focal strokes. In some patients, localized infarction occurs (Figure 3).

Neuropsychiatric assessment

The neuropsychiatric assessment starts by evaluating the severity of brain injury. In this way, the likely outcomes attributable to direct effects of brain injury can be determined, and any mismatch between these and what is observed can be attributed to psychological reactions or independent events. So, for example, in somebody with a severe psychotic illness that develops 3 months after an injury with no loss of consciousness, one can be fairly confident that the illness is not a direct consequence of the effects of brain injury on delusion formation. It is possible that the psychological trauma of the injury has allowed an acute psychotic reaction, or even that the injury was irrelevant and that the person was on the path to becoming schizophrenic anyway. On the other hand, it is likely that the psychotic illness is a direct effect of the brain injury in somebody in whom a delusional misidentification syndrome develops 3 months after an injury that was followed by coma for a week and delirium for several weeks.

The severity of brain injury is measured by the following:

  • Glasgow Coma Scale (used soon after injury)
  • Duration of loss of consciousness
  • Duration of posttraumatic amnesia (PTA), ie, the interval between the injury and the return of continuous day-to-day memories

The duration of PTA is particularly useful as a measure of the severity of the brain injury because it can be measured retrospectively, eg, in the clinic years after injury, and it is a good predictor of outcome.3 As a rule, if PTA lasts less than 1 week, a reasonably good outcome is expected. If PTA lasts longer than 1 month, significant disability is likely; a good proportion of those affected will not be able to return to work or to independent living. In general, younger individuals (those in their late teens or 20s) tend to do much better.

An MRI scan is essential in cases where the extent of damage is unclear because it may show unexpected brain injury. Gradient echo sequences are the most sensitive and should be undertaken, particularly in those with mild injury. A normal MRI scan does not rule out brain injury, but it does make significant disability as a direct effect of severe brain damage unlikely. Electroencephalography is usually not helpful, even as a predictor of posttraumatic epilepsy.

Neuropsychometric assessment can be useful in defining the severity of cognitive impairment and any areas of particular impairment. Such tests as the North American Adult Reading test are available and provide an estimate of the patient’s preinjury IQ. Such assessment is necessary for the accurate interpretation of a patient’s postinjury performance. Also, make sure that tests of executive function have been done. Note, though, that normal neuropsychometric test results do not rule out brain injury as the cause of problems with executive functions in everyday life.

Continue —> Neuropsychiatric Effects of Traumatic Brain Injury | Psychiatric Times

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