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Since the mid-1980s, the relationship between the clinical neurosciences of neurology, neuropsychology, and psychiatry has been the subject of several important textbooks that seek to cross these disciplinary boundaries.16 Lishman7 succinctly described the overlap between neurology and psychiatry as a “delicate balance … between our knowledge and understanding of the brain and our knowledge and understanding of people.” Neuropsychology, as a relative newcomer to this field, has added a third element to this balance, and the advent of new investigative imaging modalities and molecular biology technologies has further assisted in “closing the great divide.”8 At the heart of these converging relationships lies an increasing appreciation that a thorough assessment and formulation of individual patients is incomplete without reference to the knowledge and skills of other disciplines. The logical conclusion to this convergence is that disciplinary hybrids such as neuropsychiatry, behavioral neurology, and cognitive neuropsychology may be better replaced by the broader concept of a clinical neuroscience.

Although the core expertise of each discipline may differ, the clinical assessment always includes the documentation of a detailed history and the performance of an examination that is driven by a process of hypothesis testing. The major difference in assessment between disciplines is determined by their specific expertise, whether it be the neurological examination, the psychiatric mental state examination, or a detailed neuropsychological assessment. An element common to all is the assessment of cognition, which in neurological practice has been termed the mental status examination.9 In psychiatric practice, the term mental state/status examination refers to a broader assessment of the patient’s mental state and incorporates the cognitive assessment. Because most neurologists and psychiatrists are restricted to bedside assessments of patients and have limited access to neuropsychological expertise, all possible information must be incorporated into decisions regarding the patient’s cognitive abilities. The clinical skill of cognitive assessment extends far beyond the administration of a test and the generation of a score. A common error among junior clinicians is to base diagnosis on a test score and ignore the richness of cognitive information available from the remainder of their interaction with the patient.

This chapter takes a broad approach to cognitive assessment as a process that should incorporate all information available to the clinician from the moment a referral is initiated through cognitive testing to the process of feedback to the patient. Neuropsychological assessment, although seen as the “gold standard” of cognitive assessment, is not always available because of limited service resources, cost, or geographical issues. Even if neuropsychological expertise is available, it may be limited by the patient’s inability or refusal to undertake formal testing. In such situations, clinical needs may still necessitate an assessment of the patient’s cognitive state, and the clinician needs to form a judgment on the basis of all available information.


Integration of Neurobehavioral and Neurocognitive History

Neurobehavioral disturbances such as depression or psychosis are often the initial presenting feature in patients with neurocognitive impairment. Conversely, patients who initially present with the neurocognitive features of dementia may later exhibit psychotic symptoms; disinhibited, stereotypical, or inappropriate behavior; or mood and anxiety disturbance.10 Psychiatric disorders with associated behavioral disturbance may themselves manifest with neurocognitive impairments, such as the difficulties with sustained attention, memory, and processing speed seen in major depression11 or the working memory impairments seen in schizophrenia.12 Neurobehavioral impairment may herald future neurocognitive impairment, and vice versa. For example, frontotemporal dementias commonly manifest with neurobehavioral disturbance,13 and late-life depression may herald Alzheimer’s disease.14

Evolution of Symptoms

The longitudinal course of illness is most commonly established through informants, and a complete history may need to be obtained from a number of sources. The nature of the onset of symptoms and the context in which they occur may be diagnostically discriminatory. For example, delirium usually manifests rapidly over a couple of days in the context of significant medical insult, whereas neurocognitive impairment associated with a central nervous system (CNS) neoplasm usually manifests over a few months, frequently in concert with other neurological symptoms. Many caretakers of patients with a dementing illness report subtle and insidious changes occurring for a year or more before assessment. Exceptions to this may occur, such as a subacute delirium or a rapidly progressive dementia. The longitudinal course may allow diagnostic differentiation particularly within the dementias. Alzheimer’s disease and frontotemporal dementias usually show gradual progression, whereas the time course of vascular dementia is often, but not always, stepwise. Rapid cognitive decline is suggestive of a prion dementia or a potentially reversible cause such as vasculitis or neoplasia.

The sequence of symptoms can be similarly informative. Depressed mood and neurovegetative disturbance for 3 months before the onset of memory problems are likely to indicate a depressive “pseudodementia.” An initial presentation of apathy, disinhibition, or stereotypical behaviors before memory or language impairment are suggestive of a frontotemporal dementia, whereas impaired new learning as the first symptom would be more suggestive of an Alzheimer’s-type dementia.

The age at symptom onset may narrow the list of differential diagnoses. Cognitive impairment in early adult life may be associated with adult-onset forms of inherited metabolic disorders, such as leukodystrophies, but are more frequently associated with potentially reversible causes of impairment, such as CNS infections, inflammatory disorders, or neoplasia. When impairment manifests in the fourth through sixth decades, earlyonset dementias, such as frontotemporal dementia or familial Alzheimer’s disease, or the early manifestation of undiagnosed vascular disease should be considered. In later decades, most such illnesses are vascular or degenerative.

Finally, the presence of fluctuations in the mental state and functioning may provide clues to etiology. Fluctuations in the level of arousal and orientation over days are seen in delirium. Late afternoon and early evening deteriorations may reflect the “sundowning” seen in dementias, whereas episodes of undiagnosed confusion occurring over a number of months may point to a diagnosis of Lewy body dementia.

Neurocognitive Baseline

An understanding of an individual’s premorbid neurocognitive function allows an estimate of the degree and rate of decline. In impaired individuals with superior premorbid intellect, cross-sectional assessment may be within accepted norms for age. Commonly used screening instruments such as the Mini-Mental State Examination (MMSE) have a significant ceiling effect (see Chapter 2 on neuropsychological assessment) and are likely to be insensitive to this decline.15 Conversely, individuals with long-standing premorbid intellectual impairment may be incorrectly classified as suffering a degenerative process such as dementia, when in fact their neurocognitive function is stable.

Baseline function can be estimated grossly from the patient’s maximal educational and occupational attainment and from mental state features such as vocabulary and capacity for abstract thinking. A number of assessment tools for estimating premorbid intellectual function have been devised and rely on the stability of semantic language functions independent of disease or age. The most well-known and widely used is the National Adult Reading Test.16 This probes reading ability for irregular words, which has been shown to be relatively preserved in many disorders.17 Other similar tools include the Wechsler Test of Adult Reading18 and the Cambridge Contextual Reading Test.19 This issue is also addressed in Chapter 2 on neuropsychological assessment.


For the purposes of history taking, neurocognitive function is usefully categorized into the domains of attention, language, visuospatial function, memory, and executive function. Very few neurocognitive functions are discrete, however, and most functions are distributed across more than one domain: for example, remembering a list of three items relies on receptive and expressive speech, in addition to memory. The presence of any impairments in hearing and vision should be established as early as possible in an interview.


Language is the basic tool of human communication and a basic component of many cognitive abilities. Language functions are commonly ascribed to the dominant hemisphere, and because cerebral dominance for language is closely allied to handedness, it is useful to be aware of the patient’s handedness before language function is assessed. Most of the conditions that produce disorders of language affect the left hemisphere and are commonly of vascular, traumatic, neoplastic, or degenerative origin.

Disorders of language are separated into aphasia (partial or total inability to articulate ideas or comprehend spoken or written language), alexia (inability to read), and agraphia (inability to write). An understanding of the large group of aphasias has been complicated by various nomenclatures, although the most recognized is that originally proposed by Benson and Geschwind,20 which divides the group into Broca’s, Wernicke’s, global, conduction, anomic, and transcortical aphasias. This is discussed in more detail in Chapter 3.

The following questions are useful guides to areas for evaluation:

Visuospatial Functions

Visuospatial functions allow persons to orient themselves in space, enable safe locomotion, facilitate interaction with other individuals and objects, and allow for the expression and understanding of visual symbols of communication. Such functions are often related to pathology affecting the parietal cortex, which also contains contralateral motor and sensory representations of the body soma. Many disorders or diseases that disturb visuospatial functions are associated with significant motor or sensory impairment.

Visuospatial disturbance is common in dementias of all types, but it is most commonly seen with Alzheimer’s-type dementia. It is the presenting and dominant feature in the posterior variant, posterior cortical atrophy. Vascular or other acquired focal lesions of the parietal regions may also manifest with visuospatial difficulties. Aspects of visuoperceptual disturbance are discussed further in Chapter 5.

The following questions are useful guides to areas for evaluation:


Anterograde episodic memory is a general term for the registration, acquisition, storage, and subsequent retrieval of new information. Anterograde episodic memory impairment is perhaps the most common manifestation of neurocognitive disturbance. Anterograde episodic memory consists of several stages, beginning with the reception and registration of the information by a sensory modality, followed by the holding of the information temporarily in working memory (defined as the current content of consciousness); then storage in a more permanent form, which is enhanced by association with other already stored information and augmented by practice or rehearsal; and, finally, the process of retrieval. Each of these steps requires the integrity of the preceding steps, and any interruption in this hierarchy may disrupt anterograde episodic memory function. A detailed discussion of the various memory systems and their disorders is presented in Chapter 4.

Patients with dementia, particularly Alzheimer’s disease and vascular dementias, usually present to clinicians with memory disturbance before the onset of other neurocognitive or neurobehavioral disturbances. Memory impairment occurs commonly in brain disorders acquired from such causes as traumatic injury, postinfection states, and chronic exposure to CNS toxins such as alcohol.

The following questions are useful guides to areas for evaluation:

Executive Function

Executive functions are a group of complex functions that are based on the interaction with and executive control of basic processes such as attention, memory, and language. The prefrontal lobes and connected subcortical structures are crucial to the integrity of executive function, personality, and behavior. Cognitive functions that have been attributed to these networks include adaptive behavior, abstract conceptual ability, set-shifting/mental flexibility, problem-solving, planning, initiation, sequencing of behavior, and personality factors such as drive, motivation, and inhibition. Patients with the dysexecutive syndrome fail to anticipate changes, show poor planning ability, and do not learn from their errors. They are poor at self-guided learning and goal-setting, in that they perform normally on externally driven tasks but are poor at self-motivated tasks. Such patients are sensitive to interference from irrelevant stimuli, and may display both motor and cognitive perseveration. A more detailed overview of executive function and dysfunction can be found in Chapter 7.

Disorders that commonly manifest with executive dysfunction include frontotemporal dementias, traumatic brain injury, chronic alcohol abuse, and focal disease caused by vascular lesions or neoplasms. Of importance, but not as well recognized, is that patients with schizophrenia may exhibit subtle but often disabling disturbances of executive dysfunction.

The following questions are useful guides to areas for evaluation:


A thorough neurobehavioral assessment is essential for the neurocognitive history, because a number of disorders cause both psychological and cognitive dysfunction, and neurological diseases may manifest initially with psychological disturbance. Failing to recognize neurobehavioral disturbance can delay correct diagnosis, increase caregiver burden, and cause unnecessary, although relievable, suffering for patients and their families.

The neurobehavioral assessment is largely synonymous with the psychiatric “mental state examination.” In contrast to the traditional medical view of the history as a description of symptoms and the examination as a description of signs, the mental state examination includes elements of both the history and the phenomena observed by the examiner. The mental state examination includes descriptions of the patient, his or her behavior, and a summary of his or her responses to questions regarding mental phenomena. Like the cognitive assessment, mental state assessment should not be confined to only the part of the interview in which symptoms are being elicited. The patient who denies hallucinations but frequently and suddenly looks askance while muttering or overtly vocalizing can reasonably be inferred to be responding to hallucinations.

Appearance and Behavior

There is much to be gained by careful observation of the patient’s appearance, especially if the interviewer has obtained a good sense of the patient’s premorbid state. The patient’s personal grooming, dress, and general state of health provide important information about functional abilities. Even the state of the patient’s hands may reveal important information. The dry, chaffed hands of a repetitive washer, the nicotine-stained fingers of a patient with schizophrenia, and the tremor of a patient with alcohol dependence are some examples. Patients with chronic schizophrenia may be disheveled and dress unusually, with many layers of clothes or with seemingly little regard for their appearance. They may look around the room in a suspicious manner and on occasion may look for monitoring devices. Depressed patients may sit stooped, with slowing of their movements, or may be restless and agitated, rubbing and wringing their hands. Patients with a pseudodementia may find the interview too difficult and resort to frequent “I don’t know” answers. Anxious patients are visibly anxious, sweaty, and restless. Patients with a dysexecutive syndrome may make inappropriate sexual suggestions or be impulsive. The presence of abnormal movements or postures during the interview may be more informative than when the patient is being examined formally. The patient’s interactions with the examiner, administrative staff, or nursing staff may provide invaluable information.


Mood is the sustained level of emotional tone, whereas affect refers to the patient’s emotional behavior. The emotional response of the examiner to the patient provides a further indicator of the patient’s emotional state. Patients with disorders of mood such as major depressive disorder often show impairments in attention and psychomotor speed.21,22 Bipolar disorder is associated with impairments in attention, verbal memory, and executive function. High rates of comorbid mood disturbance are associated with Parkinson’s disease,23 Huntington’s disease,24 and multiple sclerosis.25 Late-onset depression is being increasingly seen as a prodrome to the dementias.14

Inquiries about a patient’s mood state may include the following:

“How have you been feeling recently?”

“Do you have periods of time when you are always down?”

In patients with speech disorders, responding to such questioning may not be possible, and close informants can be asked directly, “Does he/she seem unhappier to you than usual?” Informants are able to comment on the reactivity of mood, inasmuch as depressed patients are often unable to “brighten up.” Patients who are depressed may describe themselves as feeling sad, unhappy, hopeless, useless, blue, or “flat.” This mood state is often accompanied by disturbances in sleep, appetite, concentration, and motivation. The depressed patient conveys sadness and misery or presents as anxious and irritable. Commonly used tools for rating the severity of depressive symptoms include the patient-rated Beck Depression Inventory26 and the clinician-rated Hamilton Depression Rating Scale.27 Patients with elevated mood states display euphoria, elation, and irritability in association with overactivity, accelerated thoughts, disinhibited behavior, reduced sleep, and grandiose ideas. Examiners who find themselves regularly suppressing a smile or giggle in interviews with patients should always ask themselves whether the patient’s mood is elevated. Reduced intensity and narrowing of affective responses is termed blunting of affect and is a key feature of schizophrenia.


Anxiety, a normal and adaptive component of human psychological function that allows for the identification of danger or threat, may become inappropriate and/or excessive. Anxiety disorders include panic disorder, characterized by panic attacks (discrete, relatively brief periods of intense anxiety accompanied by somatic symptoms of sympathetic drive), agoraphobia (recurrent fear of inability to escape from situations such as being in a crowd or an enclosed area), social anxiety (fear of social situations), specific phobia (of a discrete object, such as heights or water), and generalized anxiety, which leads to diffuse anxiety on most days.28 Pathological anxiety states have been associated with stroke,29 Huntington’s30 and Parkinson’s diseases,31 temporal lobe epilepsy,32 and thyrotoxicosis.33 A history of anxiety can be sought through inquiries about increasing or frequent worrying, its source, and the presence of concomitant physiological signs such as sweating, tachycardia, shortness of breath, and tremor and whether the degree of worry seems excessive to the patient or caretaker.

An anxiety disorder with a strong relationship to neurological disorders is obsessive-compulsive disorder, which is associated with intrusive recurrent thoughts (obsessions) and repetitive behaviors or mental acts (compulsions such as counting, checking, or cleaning). Obsessive-compulsive disorder has been strongly associated with Gilles de la Tourette syndrome34 and with the pediatric neuropsychiatric disorder pediatric autoimmune neuropsychiatric disorder associated with group A streptococci (PANDAS).35 Symptoms of obsessive-compulsive disorder can be ascertained by questions about compulsive behaviors, such as “Do you find yourself checking/cleaning things more than once or more often than you need to?”, and obsessions, such as “Do you have recurrent, intrusive thoughts/ideas/images/impulses?”

Severe anxiety states can lead to depersonalization and derealization. These conditions can be difficult for patients to describe, but descriptions can be elicited by asking the following questions:

“Have you ever had the sense that the world around you is different or changed?” (derealization)

“Have you ever felt detached from the world around you or as if you are an observer of yourself?” (depersonalization)

Both these states may be described by patients in the prodrome of complex partial seizures, although are most commonly seen in patients with anxiety or panic disorders. Patients with panic disorder describe symptoms lasting many minutes with a buildup of anxiety symptoms such as a sense of fear, palpitations, hyperventilation, and perioral numbness. The symptoms associated with complex partial seizures are usually stereotyped and much briefer than those seen in panic disorder.

Thought Content and Form

In a number of neurological disorders, patients may develop abnormalities in their beliefs about themselves or the environment around them. Thought content can be seen as a spectrum from normal, reality-based thinking to delusions, which are fixed false ideas out of keeping with the patient’s cultural background or education.28 Delusions are categorized by the nature of their content, such as persecutory, grandiose, somatic, and erotomanic delusions or delusions of jealousy or reference. Delusions are classically associated with schizophrenia but are seen in patients with Huntington’s disease, temporal lobe epilepsy, leukodystrophies, systemic lupus erythematosus, and most forms of dementia.36 Persecutory delusions are commonly seen in delirium and substance intoxication. Organic delusions are particularly associated with diseases affecting the limbic system.37 In schizophrenia, delusions tend to be very well systematized (generally static and supported by an extensive belief system) and often have a bizarre nature, whereas in neurological disorders they are often poorly systematized and are predominantly persecutory.38

Informants may provide the most valid and reliable history about delusional ideas, although they may be unaware of them if the patient has not voiced his or her beliefs. It is useful to directly but gently inquire about delusional ideas, using questions such as “Sometimes people feel that they are being watched, that others are planning to hurt them, or that they have special abilities that other people don’t. Have you ever felt like that?”

Mood or anxiety disorders are associated with altered thought content. Depression is associated with thoughts such as “Everything seems black,” “I will not get better,” or “Life is not worth living” or with suicidal ideas. Mania is associated with thoughts such as “I am immortal,” whereas anxious patients may express thoughts such as “Something terrible is going to happen.” Suicidal ideation or other thoughts involving harm should always be carefully asked about and documented, including ideas, plans, and intent. When patients clearly express all three, the patient can be seen to be at grave risk of acting on these ideas and usually requires hospitalization.

Thought form refers to the structure of thought and is necessarily conveyed through speech. The form of thought may be fragmented and interspersed with pauses in the delirious patient. Thoughts that progressively veer away from the question (tangentiality) or that do not follow logically from each other (loosening of associations) are almost pathognomonic of schizophrenia. The manic patient with flight of ideas displays a flow of thought that is rapid and determined by factors other than the logical flow of ideas, such as the sounds of words (clanging).


Perceptual experience occurs on a continuum, with “true” perception of stimuli at one end and frank hallucinations at the other.39 Hallucinations are defined as percept-like experiences in the absence of an external stimulus that are spontaneous and unwilled and cannot be readily controlled.40 Illusions, which are distortions or elaborations of a normal stimulus, also belong to this continuum. Hallucinations can be well formed and complex or poorly formed and simple,41 and they are categorized according to sensory modality. Complex and elaborate auditory hallucinations are the hallmark of schizophrenia but can occur in severe affective psychotic states. Poorly formed, fragmented auditory hallucinations may be present in organic states such as delirium. Special note should be made of complex visual hallucinations, which are often a feature of organic states. Examples include the Charles Bonnet syndrome and peduncular hallucinosis, where lesions to the visual pathways and to their terminations or ascending inhibitory afferent pathways, respectively, can result in strikingly vivid formed scenes, complex patterns, or groups of miniature figures or animals.42 Olfactory, gustatory, and tactile hallucinations are not commonly experienced in psychiatric illness and should alert the clinician to the possibility of neurological conditions such as complex partial seizures or neoplasia. For patients who are reluctant or unable to discuss their experiences, questioning caretakers about behavior that might represent a reaction to perceptual disturbance, such as responding to voices or gaze movements in response to visual phenomena, may prove useful.

Vegetative Function

Vegetative functions such as sleep, appetite, and sexual drive are often disturbed in patients with neurobehavioral disturbances, particularly disturbances of mood.43 Patients may complain of appetite disturbance with weight loss or gain; sleep disturbance with insomnia in initial, middle, or terminal sleep phases (the last known as early morning wakening, a characteristic of severe depression); altered libido; disturbances in energy and motivation; and impaired capacity to enjoy usual pursuits.

Insight and Judgment

A patient’s lack of insight into illness may reduce the validity of a history, such as the patient’s self-report of memory complaints44 or of adherence to prescribed treatments.45 Insight has been traditionally viewed in both psychological and cognitive frames. In the psychological frame, insight relates to acceptance of illness and the need for its treatment. Insight is impeded by denial of illness, which occurs to varying degrees and reflects psychological coping mechanisms that allow the patient to deal with the fear, hopelessness, or shame associated with sickness and its treatment.46 Cognitive models focus on the neurocognitive capacity of an individual to internalize, retain, and cognitively process the awareness of symptoms, attribute these to an illness, and appreciate the likely effects of accepting or refusing treatment.47 Cognitive models of insight were devised from the strong association of disorders in which disrupted frontal-executive function is the cognitive hallmark, such as frontotemporal dementia and schizophrenia, with poor insight.45,48 An apparent change in insight is likely to reflect an organic process, inasmuch as the psychological mechanisms that relate to insight tend to be personality based and thus relatively stable.49

The concept of insight overlaps with the neurological symptom of anosognosia, a lack of awareness of neurological deficit, first described by Babinski50

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