A useful conceptual framework for a comprehensive neu-ropsychiatric assessment is the biopsychosocial model.
The biopsychosocial model integrates clinical data from three interrelated domains: 1) biological disturbances in brain function; 2) the patient’s emotional and psycholog-ical reactions to impairments in cognition and distur-bances of behavior, including his or her awareness and acceptance of the impairments; and 3) disruptions of interpersonal relationships, family interactions, and work capacities. A comprehensive, integrated clinical
assess-ment based on such a framework leads to the identifica-tion of specific problem areas, a multidimensional formu-lation of etiology, and development of treatment approaches that focus specifically, yet comprehensively, on the patient’s problems.
History Related to the Brain Injury and Recovery Period
There are a number of questions that are relevant to the neuropsychiatric assessment of the patient with TBI (Table 4–1). Traditionally, the clinical database begins with the elicitation of the patient’s chief complaint, which may or may not include a spontaneous report of a history of TBI. Gordon et al. (1998) describe “The Enigma of
‘Hidden’ Traumatic Brain Injury,” noting that TBI may be “hidden” in three senses: 1) the diffuse axonal injury (DAI) of mild TBI is rarely detected by brain imaging, 2) the effects of TBI are usually not obviously physical, and 3) individuals with TBI are often unaware that signif-icant problems have occurred as a result of the injury.
Because TBI is often “the invisible injury,” the history of TBI may elude both the examiner and the patient; there-fore, the clinician must specifically inquire about events that may be associated with TBI such as motor vehicle accidents (MVAs), falls, assaults, and sports or recre-ational injuries.
Once a history of TBI is obtained, it is useful to de-lineate the type, severity, and location of the injury and when it occurred. Several parameters are commonly used to ascertain the severity of injury, including the Glasgow Coma Scale (GCS), duration of loss of con-sciousness (LOC), and posttraumatic amnesia (PTA)
(Table 4–2). Because the survivor of a TBI does not know whether he or she was rendered unconscious by the trauma, it is important to verify LOC with a witness, if possible. The survivor may believe that LOC occurred when, in actuality, he or she was conscious but in a state of PTA. Introduced by Teasdale and Jennett (1974), the GCS (see Table 1–2 in Chapter 1, Epidemiology) has become the standard for measuring the acute severity of a TBI. Estimating the severity of an acute TBI guides the physician in quantifying the signs and symptoms
as-sociated with mild, moderate, or severe TBI as well as the patient’s likely prognosis. According to Asikainen et al. (1998), the GCS score and duration of LOC and PTA all have strong predictive value in assessing functional or occupational outcome for TBI patients. However, Lov-ell et al. (1999) question the predictive value of LOC based on the lack of statistical correlation between LOC and neuropsychological functioning in a large sample of patients with mild head trauma.
A temporal relationship should be established be-tween the onset of current signs and symptoms and the occurrence of the traumatic injury. This information helps to differentiate the premorbid personality charac-teristics and psychiatric and behavioral symptoms from those arising after the brain injury. Any number of emo-tional and behavioral difficulties that existed in milder form before the brain injury can be accentuated after it.
Careful consideration of temporal relationships also must address the phase of recovery and associated behavioral changes, because improvement after TBI tends to occur along a continuum, with certain sequelae generally re-solving before others (e.g., confusion and disorientation generally resolve before short-term memory impair-ment). The clinician should also focus attention on the patient’s psychological reactions and adjustment to injury-induced cognitive and emotional changes, as well as their impact on interpersonal relationships, family dynamics, and employment status.
In the assessment of TBI, it is helpful to categorize observed signs and symptoms into the broad domains of cognition, emotion, behavior, and physical symptoms (Table 4–3). This categorization permits more precise di-agnosis of the patient’s problems and assists in the formu-lation of an optimal treatment plan.
Importance of Collateral History
Because insight into disturbances of cognition, behavior, and emotional state are often compromised in patients T A B L E 4 – 1 . Sample questions for traumatic brain
injury (TBI) assessment
Questions Rationale
Have you ever hit your head?
Have you ever been in an accident?
Probe for car/motorcycle/
bicycle/other motor vehicle accidents, falls, assaults, sports or recreational injuries (If so) Did you black out, pass
out, or lose consciousness?
Establish LOC (verify LOC with witness, if possible) What is the last thing you
remember before the injury?
Establish extent of retrograde amnesia
What is the first thing you recall after the injury?
Estimate duration of LOC and begin to quantify
posttraumatic amnesia (must ask further about when contiguous memory function returned)
(If no LOC) At the time of the injury, did you experience any change in your thinking or feel “dazed” or
“confused”?
Establish change in mentation or level of consciousness
What problems did you have after the injury?
Delineate post-TBI symptoms (see Table 4–3)
Has anyone told you that you’re different since the injury? If so, how have you changed?
Detect problems outside survivor’s awareness or those he/she may be minimizing
Did anyone witness or observe your injury?
Identify source of collateral history
Many people who have injured their head had been drinking or using drugs; how about you?
Offer survivor greater
“permission” to admit substance use
Have you had any other injuries to your head or brain?
Identify previous TBIs that may increase morbidity from current injury
Note. LOC=loss of consciousness.
T A B L E 4 – 2 . Classification of traumatic brain injury (TBI)
Type of TBI
Glasgow Coma
Scale
Loss of consciousness
Posttraumatic amnesia Mild 13–15 30 minutes or less
(or none)
<24 hours
Moderate 9–12 30 minutes to 1 week
>24 hours to <1 week
Severe ≤8 >1 week >1 week
with brain injury, it is incumbent on the clinician to verify from collateral sources the accuracy of the patient’s account of his or her history and symptomatology. In cases of severe TBI, patients rarely recall the incidents surrounding the injury. This disturbance in recall of the incident itself, in conjunction with the patient’s decreased awareness of his or her deficits, makes accessing collateral information essential. Collateral history may be obtained from a variety of sources (Table 4–4), including family and friends who can describe changes in behavior, cognition, personality, and general level of functioning since the brain injury.
Collateral history is also pivotal because survivors of TBI and their families and friends see the injuries through different lenses. For example, Sbordone et al. (1998) found that patients with TBI generally underreported cognitive, behavioral, and emotional symptoms as compared to those reported by significant others, regardless of the severity of injury. For example, 58.8% of significant others in the study noted emotional lability or mood swings in the pa-tients with TBI, whereas only 5.9% of the papa-tients re-ported such difficulties. Circumstantiality was observed by 29.4% of significant others; but none of the patients re-ported such problems. In those with severe TBI, none of the patients recognized problems with judgment, whereas 45% of their significant others identified this problem.
Hospital records related to the acute treatment of a TBI provide invaluable information about the traumatic event. This information includes the nature of the
trauma (e.g., MVA, fall, or blunt trauma); severity (GCS, period of unconsciousness, presence of traumatically re-lated seizures, duration of retrograde amnesia and PTA, medical complications, and course of recovery); time of onset and types of neurobehavioral changes that oc-curred during the acute and postacute phases of recov-ery; and results of neuroimaging, electrophysiological, and neuropsychological testing delineating the location and extent of injury and pattern of cognitive and mem-ory impairment associated with it. Medical and psychi-atric records for the period before the trauma are also helpful in relating current signs and symptoms to past psychiatric disturbances and premorbid personality, and can assist in ascertaining the relative contributions of T A B L E 4 – 3 . Traumatic brain injury symptom checklist
Cognitive Emotional Behavorial Physical
Level of consciousness Mood swings/lability Impulsivity Fatigue
Sensorium Depression Disinhibition Weight change
Attention/concentration Hypomania/mania Anger dyscontrol Sleep disturbance
Short-term memory Anxiety Inappropriate sexual behavior Headache
Processing speed Anger/irritability Lack of initiative Visual problems
Executive function (planning, abstract reasoning, problem-solving, information processing, ability to attend to multiple stimuli, insight, judgment, etc.)
Apathy “Change in personality” Balance difficulties
Dizziness Coldness
Change in hair/skin
Thought processes Seizures
Spasticity
Loss of urinary control Arthritic complaints Source. Adapted from Hibbard MR, Uysal S, Sliwinski M, et al: “Undiagnosed Health Issues in Individuals With Traumatic Brain Injury Living in the Community.” The Journal of Head Trauma Rehabilitation 13:47–57, 1998.
T A B L E 4 – 4 . Sources of collateral history
People Documents
Family Police reports
Friends Emergency medical service reports
Co-workers Medical records
Witnesses to injury Educational history Medical staff Driving record Allied health professionals
(occupational, physical, and speech therapists, etc.)
antecedent variables, the brain injury itself, and current psychosocial parameters to observed neurobehavioral changes.
If available, posttrauma psychiatric and/or rehabilita-tion records help delineate the course of the patient’s re-covery, including the acute versus chronic nature of pre-senting psychiatric complaints, and provide a source of additional behavioral observations. Relevant posttrauma records also should be reviewed for the emergence of sub-sequent medical problems, results of neurodiagnostic studies, and indications of the efficacy and adverse effects of various treatment interventions the patient may have received. Additional sources of collateral information that may prove helpful include police reports and emergency medical service records (to provide information about the accident and condition of the patient at the scene), educa-tional records, and driving record (to provide a history of prior MVAs).
Current Neuropsychiatric Symptoms
Within days of a mild to moderate TBI, a significant num-ber of patients experience headaches, fatigue, dizziness, decreased attention, memory disturbance, slowed speed of information processing, and distractibility (Levin et al.
1987b; McLean et al. 1983). Other symptoms that fre-quently occur within the first few days after such an injury include hypersensitivity to noise and light, irritability, easy loss of temper, sleep disturbances, and anxiety (Binder 1986). These symptoms, which are often referred to as
“postconcussive” symptoms, are described in more detail in Chapter 15, Mild Brain Injury and the Postconcussion Syndrome.
Although there are some discrepancies in the results of available follow-up outcome studies, it is apparent that most patients experience substantial resolution of cognitive, somatic, and emotional symptoms within 1–6 months after a mild brain injury (Barth et al. 1983;
Rimel et al. 1981). However, there is a significant sub-group of patients who continue to experience difficulties with reasoning, information processing, memory, vigi-lance, attention, and depression and anxiety (see Chap-ter 17, Cognitive Changes).
The symptom profile with moderate TBI is generally similar to that seen with mild TBI, but the frequency of symptoms is greater, and they tend to be more severe (Rimel et al. 1982). Severe TBI is associated with a large number of chronic neurobehavioral changes, acute as well as delayed in onset (Table 4–5). Recovery from severe TBI is typically marked by a number of stages that can be documented using the Rancho Los Amigos Cognitive Scale (Table 4–6).
Severe TBI
A common sequence of stages has been identified in the recovery from severe TBI. It is important to note that not everyone follows this sequence. For example, one may reach a particular stage and fail to progress further, or one may demonstrate features of different stages simultaneously.
The first stage of recovery after a severe TBI is coma, which is characterized by LOC and unresponsiveness to the environment. A simple but useful measure of the depth of coma is the GCS. On emerging from deep coma, the patient enters the second stage of recovery, a state of unresponsive vigilance, marked by apparent gross wake-fulness with eye tracking, but without purposeful respon-siveness to the environment. The third stage of recovery is characterized by mute responsiveness, in which there T A B L E 4 – 5 . Neurobehavioral symptoms
associated with severe brain injury
Relative frequencies during postinjury period (%) Symptoms 6 months 12 months 2 years
Forgetfulness — — 54
Slowness 69 69 33–65
Tiredness 69 69 28–30
Irritability 69 53–71 38–39
Memory problems 59 69–87 68–80
Decreased initiative — 53 —
Impatience 64 57–71 —
Anxiety 66 58 16–46
Temper outbursts 56 50–67 28
Personality change 58 60 —
Depressed mood 52 57 19–48
Headaches 46 53 23
Childishness — — 60
Emotional lability — — 21–40
Restlessness — — 25
Poor concentration — — 33–73
Lack of interest — — 16–20
Dizziness — — 26–41
Light sensitivity — — 25
Noise sensitivity — — 23
Source. Adapted from Jacobs 1987; Mauss-Clum and Ryan 1981;
McKinlay et al. 1981; Thomsen 1984; and Van Zomeren and Van Den Berg 1985.
are no vocalizations, but the patient responds to com-mands. Identification of this stage depends on demonstrat-ing the patient’s capacity to carry out simple commands that will not be confused with reflex activity and do not depend on intact language function, because the patient may have an aphasia or apraxia. Requesting that the pa-tient carry out various eye movements is often the best task to use, and the movements can range from simple to complex (Alexander 1982).
The next phase of recovery is characterized by the re-turn of speech and language function. During this stage, the patient begins to demonstrate a confusional state akin to delirium as indicated by fluctuating attention and con-centration and an incoherent stream of thought (see Chap-ter 9, Delirium and Posttraumatic Amnesia). The confused or delirious patient usually displays distractibility, persever-ation, and a disturbance in the usual sleep/wake cycle. Such
patients may become agitated and demonstrate increased psychomotor activity. This stage is also frequently associ-ated with sensory misperceptions, hallucinations, confabu-lation, and denial of illness (Alexander 1982).
During the stage of confusion, the patient is not able to form new memories in a normal fashion and is disori-ented. This stage is the period when posttraumatic anter-ograde amnesia is prominent. PTA is considered to be present until the patient is consistently oriented and can recall particulars of his or her environment in a consis-tent manner. The duration of PTA can be assessed with the Galveston Orientation and Amnesia Test (GOAT) (Levin et al. 1979a, 1979b) (see Figure 8–1 in Chapter 8, Issues in Neuropsychological Assessment), which moni-tors both the degree of orientation and recall of newly learned material. The length of PTA is one of the best in-dicators of the severity of injury and is a clinically useful predictor of outcome. Furthermore, the length of PTA may correlate with the occurrence of psychiatric and be-havioral sequelae.
When the stage characterized by PTA resolves, atten-tion and concentraatten-tion improve, confabulaatten-tion lessens, and the sleep/wake cycle normalizes, although problems often persist with daytime fatigue and insomnia. These changes mark a major transition from the acute to the subacute and chronic phases of recovery. This transition phase is characterized by persistent, though less severe, disturbances in attention, concentration, memory impair-ments, and limited awareness of the presence of other dis-turbances of cognitive function. Some patients also experi-ence retrograde amnesia, which rapidly shrinks and is usually relatively short in duration.
As the chronic phase of recovery unfolds, changes in personality, behavior, and emotions may emerge and be su-perimposed on the cognitive disturbances. Many patients with severe TBI complain of forgetfulness, irritability, slowness, poor concentration, fatigue, and dizziness, in ad-dition to headache, mood lability, apathy, depressed mood, and anxiety (Hinkeldey and Corrigan 1990; Thomsen 1984; Van Zomeren and Van Den Burg 1985).
Signs and Symptoms After TBI
The types of signs and symptoms that may occur after a TBI of any severity are, in part, related to the type of injury (diffuse or focal) and its anatomical location.
Symptoms that are thought to be associated with DAI include mental slowness, decreased concentration, and decreased arousal (Alexander 1982; Gualtieri 1991).
Symptoms after TBI are often linked to lobar or regional areas of the brain (frontal lobe syndromes or temporal lobe syndromes). Although such models lend convenience and T A B L E 4 – 6 . Rancho Los Amigos Cognitive Scale
I. No response: Unresponsive to any stimulus II. Generalized response: Limited, inconsistent, and
nonpurposeful responses—often to pain only III. Localized response: Purposeful responses; may follow
simple commands; may focus on presented object IV. Confused, agitated: Heightened state of activity;
confusion, and disorientation; aggressive behavior;
unable to perform self-care; unaware of present events;
agitation appears related to internal confusion V. Confused, inappropriate: Nonagitated; appears alert;
responds to commands; distractible; does not concentrate on task; agitated responses to external stimuli; verbally inappropriate; does not learn new information VI. Confused, appropriate: Good directed behavior, needs
cuing; can relearn old skills as activities of daily living;
serious memory problems, some awareness of self and others
VII. Automatic, appropriate: Appears appropriately oriented;
frequently robotlike in daily routine; minimal or absent confusion; shallow recall; increased awareness of self and interaction in environment; lacks insight into condition;
decreased judgment and problem solving; lacks realistic planning for future
VIII. Purposeful, appropriate: Alert and oriented; recalls and integrates past events; learns new activities and can continue without supervision; independent in home and living skills; capable of driving; defects in stress tolerance, judgment, and abstract reasoning persist; may function at reduced levels in society
Source. Reprinted with permission from the Adult Brain Injury Service of the Rancho Los Amigos Medical Center, Downey, California.
order to the understanding of the sequelae of TBI, they may be too simplistic because individuals often present with symptoms from several regions. Neuropsychiatric symptoms may be more closely linked to circuits that connect a number of lobes and regions involved in sim-ilar functions. Although it may not be possible to link structural lesions with symptoms based on anatomical lo-cation alone, the following syndromes are classic.
Focal lesions involving the convexities of the frontal lobes (or, more likely, frontal lobe circuitry) are typically associated with decreased initiation, decreased interper-sonal interaction, passivity, mental inflexibility, and perse-veration. Focal lesions involving the orbitofrontal surfaces are associated with disinhibition of behavior, dysregulation of mood and anger, impulsivity, and sexually and socially inappropriate behavior (Cummings 1985; Gualtieri 1991;
Mattson and Levin 1990).
Temporal lobe lesions are often associated with mem-ory disturbances (left-sided lesions interfering with verbal memory and right-sided lesions with nonverbal memory), increased emotional expressiveness, uncontrolled rages, sudden changes in mood, unprovoked pathological crying and laughing, manic symptoms, and delusions (Gualtieri
1991). Bilateral temporal lobe injuries may cause a Klüver-Bucy–like syndrome, characterized by placidity, hyperoral-ity, increased exploratory behavior, memory disturbance, and hypersexuality (Cummings 1985; Gualtieri 1991).
Some of the signs and symptoms of TBI result from the patient’s emotional and psychological responses to having experienced a TBI and having to deal with its neg-ative interpersonal and social consequences. Patients with TBI may experience frustration, anxiety, anger, depres-sion, irritability, isolation, withdrawal, and denial in re-sponse to the losses they have experienced. The array of psychiatric and behavioral symptoms demonstrated by patients with TBI do not always cluster in a syndromically defined fashion (with the possible exception of the post-concussive syndrome in mild TBI), nor do they always al-low for a specific diagnosis based on DSM-IV-TR criteria (American Psychiatric Association 2000). Table 4–7 shows common DSM-IV-TR diagnoses used in TBI-re-lated neuropsychiatric sequelae.
According to a number of studies, TBI appears to be a risk factor for a number of psychiatric disorders, including major depression, dysthymia, obsessive-compulsive disor-der, phobias, panic disordisor-der, alcohol or substance abuse/de-T A B L E 4 – 7 . Traumatic brain injury (TBI)–related DSM-IV-TR disorders
TBI sequelae DSM-IV-TR disorders
PTA Delirium due to TBI (293.0)
Persistent global cognitive impairments in context of intact sensorium (after resolution of PTA)
Dementia due to TBI, with or without behavioral disturbance (294.11 and 294.10, respectively)
“Postconcussive” syndrome Cognitive disorder not otherwise specified (294.9) (research criteria specific for
“postconcussional disorder” in Appendix B) Isolated impairment of memory Amnestic disorder due to head trauma (294.0)
Changes in personality Personality change (apathetic, disinhibited, labile, aggressive, paranoid, other, combined, unspecified) due to TBI (310.1)
Persistent hallucinations, delusions Psychotic disorder (with delusions or hallucinations) due to TBI (293.81 and 293.82, respectively)
Persistent depression, mania Mood disorder (with depressive, major depressive-like, manic, or mixed features) due to TBI (293.83)
Persistent anxiety symptoms Anxiety disorder (with generalized anxiety, panic attacks, or obsessive-compulsive symptoms) due to TBI (293.84)
Impaired libido, arousal, erectile dysfunction, anorgasmia, etc.
Sexual dysfunction due to TBI: female or male hypoactive sexual desire (625.8 and 608.89, respectively); male erectile disorder (607.84); other female or male sexual dysfunction (625.8 and 608.89, respectively)
Insomnia, reversal of sleep-wake cycle, daytime fatigue, etc.
Sleep disorder due to TBI (780.xx): insomnia type (.52); hypersomnia type (.54);
parasomnia type (.59); mixed type (.59) Note. PTA=posttraumatic amnesia.
Source. Adapted from American Psychiatric Association: Diagnostic and Statistical Manual of Mental Disorders, 4th Edition, Text Revision. Washing-ton, DC, American Psychiatric Association, 2000.
pendence, bipolar disorder, and schizophrenia (Hibbard et al. 1998a; Silver et al. 2001), although the incidence of bipo-lar disorder and schizophrenia after TBI is much less fre-quent than depression and select anxiety disorders. Other psychiatric disorders commonly seen after TBI include generalized anxiety disorder (Jorge et al. 1993), posttrau-matic stress disorder (Bryant and Harvey 1999; Hibbard et al. 1998a), psychosis (Fujii and Ahmed 2001), attention-deficit/hyperactivity disorder, conduct disorder, and oppo-sitional defiant disorder (Max et al. 1998). The incidence of comorbidity is also high, especially for major depression, anxiety disorders, and substance use disorders, as noted by Hibbard et al. (1998a) in a study of 100 adults with TBI in which 44% of patients met criteria for two or more Axis I disorders. In another study of 100 individuals with TBI fo-cused on identifying Axis II pathology, Hibbard et al. (2000) found that 66% of patients met criteria for at least one per-sonality disorder, most commonly borderline, avoidant, paranoid, obsessive-compulsive, and narcissistic types.
Given the significant burden of both Axis I and II pathol-ogy, it is not surprising that those patients with TBI have a greater lifetime prevalence of suicide attempts (nearly four times that of individuals without a history of TBI) and poorer quality of life, according to Silver et al. (2001).
Neurological Symptoms
Brain injuries cause a number of subtle as well as gross neu-rological disturbances, including visual and sensory distur-bances, motor dysfunction, ataxias, tremor, aphasias, aprax-ias, and seizures. Inquiring about neurological symptoms and a careful neurological examination may shed light on the nature and extent of brain injury and associated focal neurological dysfunction. However, it is important to note that the neurological examination may be entirely normal despite the presence of a TBI because the examination focuses primarily on sensorimotor function.
The neurological examination (Table 4–8) should as-sess various aspects of motor function, such as strength, tone, gait, cerebellar function (ataxia), fine motor move-ments (speed and coordination), motor imitation, and re-flexes. Vision should be tested to identify any field cuts or diminished acuity. Sensory function, including the sense of smell, should also be examined. Although infrequently detected, anosmia (the impairment of the sense of smell) is a common sequela of TBI often associated with nega-tive functional outcomes related to orbitofrontal damage and executive function deficits (Callahan and Hinkebein 1999). Because the olfactory nerves are located in close proximity to the orbitofrontal cortex, anosmia may serve as a marker for frontal lobe deficits. Frontal lobe damage or dysfunction may also be indicated by the presence of frontal release signs, including the grasp reflex, glabellar
blink reflex (Meyerson’s sign), Hoffmann’s sign, palmo-mental reflex, and suck, snout, and rooting reflexes.
In addition to focal neurological disturbances after TBI, there is growing concern that TBI may be a risk factor for the later development of neurological illnesses, including Alzheimer’s disease (see Chapter 28, Elderly) and multiple sclerosis (MS). The association between trauma and MS has been debated in the literature for many years. Multiple stud-ies have demonstrated that central nervous system (CNS) trauma disrupts the blood-brain barrier (BBB), allowing pas-sage of blood components that deliver the instruments of in-flammation to the brain (Poser 2000). Lehrer (2000) notes that cytokines released by TBI disrupt the BBB and precipi-tate exacerbation in MS. Other investigators disagree and suggest that brain inflammation may cause a secondary change in the BBB rather than the opposite (Cook 2000). Al-though Cook acknowledges the possibility of a slight adverse effect on the course of MS after trauma, he states that there is no convincing evidence that physical trauma causes MS. In addition, the preponderance of evidence reviewed by the Therapeutics and Technology Assessment Subcommittee of the American Academy of Neurology reveals no association between physical trauma and either MS onset or MS exac-erbation (Goodin et al. 1999).
Patients with severe TBI may experience impairment in expressive speech and receptive language function (post-traumatic aphasias), which may be indicated by deficits in naming, repetition, and word fluency (Levin et al. 1976;
Sarno 1980). Patients with frontal lobe lesions may pro-duce speech that is simple in structure and poorly orga-nized. Patients with orbitofrontal damage may demon-strate confabulation and digressive speech, whereas patients with left dorsolateral lesions may have linguistic deficits, marked perseveration, and difficulty initiating speech (Kaczmarek 1984).
T A B L E 4 – 8 . Neurological examination after traumatic brain injury: key areas of assessment
Sensory Motor Other
Vision (look for field cuts)
Strength, tone, gait (r/o ataxia)
Aphasia, confabulation, perseveration Smell (r/o
anosmia)
Fine motor movements, speed, coordination (observe for tremor)
Seizures
Frontal release signs Recognition
(r/o agnosia) Motor imitation (r/o apraxia)
Reflexes Note. r/o=rule out.