Neurologic disorders associated with behavioral symptoms …

M Justin Coffey MD

General Neurology

Updated 08.28.2024
Released 03.09.2010
Expires For CME 08.28.2027

Neurologic disorders associated with behavioral symptoms

Author: M Justin Coffey MD

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Editor: Howard S Kirshner MD

Neurologic disorders associated with behavioral symptoms

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Introduction

Overview

Behavioral disturbances occur in most patients with neurologic disease and are substantial factors determining quality of life for such patients. Most of these difficulties can be treated safely and effectively. Yet behavioral signs and symptoms may go unnoticed or are minimized, incorrectly ascribed to a preexisting psychiatric disorder, or misunderstood as “psychogenic” in origin. Working knowledge of brain-behavior relations helps clinicians understand associated behavioral disturbances as evidence of brain dysfunction. This article relies on descriptive psychopathology to outline common disturbances in various behavioral domains and to consider their diagnostic implications.

Key points

	• Behavioral disturbances due to primary neurologic conditions can be distinguished from idiopathic psychiatric disease by applying principles of brain-behavior relationships.
	• Functional brain systems, when disturbed, have signature psychopathology.
	• Recognizing behavioral disturbances that represent distinct neuropsychiatric syndromes informs diagnostic and treatment considerations.

Clinical manifestations

Presentation and course

Principles of descriptive psychopathology. All human behavior is generated by the brain. Unlike some neurologic signs (eg, hemiparesis, Broca aphasia), most behavioral signs and symptoms do not localize in traditional ways to specific anatomic brain sites. The behaviors do, however, reflect dysfunction in specific brain systems or are strongly associated with specific brain syndromes. The clinical challenge is discerning which behavioral disturbances represent primary neurologic disease and which represent idiopathic psychiatric disease. Current classification systems (Diagnostic and Statistical Manual of Mental Disorders-IV-TR [DMS]; International Classification of Diseases-10 [ICD]) offer insufficient help in this regard because their diagnostic categories lack pathophysiologic and prognostic validity, and applying their diagnostic criteria may not inform treatment (49; 30).

Applying an understanding of brain-behavior relationships, however, strengthens the recognition of psychiatric illness when the pattern of psychopathology is ambiguous (eg, frontal lobe apathy syndrome vs. depressive illness; frontal lobe disinhibition syndrome vs. mania). It also helps identify neurologic disease when it is expressed mostly as psychopathology (eg, psychosis due to a stroke outside the motor system; bizarre or disruptive social behaviors in persons with partial complex seizures). In this article, we characterize common behavioral disturbances associated with neurologic practice, how their presence distinguishes neurologic from psychiatric illness, and their implications for prescribing specific treatments.

Psychopathology in different behavioral domains and its associated neurologic disease.

Disturbances in emotional expression. Disturbances in emotional expression are two to three times more common in patients with neurologic conditions than in control or reference populations, especially among the elderly (09). Distinguishing these states from idiopathic psychiatric illness is difficult when clinicians use descriptors like “depression” and “anxiety,” which also refer to emotional states experienced by all non-ill persons. On the other hand, the emotional expressions of pathologic states such as melancholia, apathy, and mania are subjectively and objectively distinct.

Melancholia is a pathologic emotional state strongly associated with mortality from suicide and with positive responses to specific treatments (46), making it the most important emotional disturbance for clinicians to distinguish from demoralization, depression associated with personality deviation, and apathy from frontal circuitry disease. Unlike these other conditions, melancholia is often accompanied by psychosis and catatonia. Patients may also appear demented (a reversible “pseudodementia”). Mania is rarely seen in neurologic practice, but chronic hypomania is important to distinguish from frontal disinhibition syndromes. The features of melancholia (Table 1) and hypomania (Table 2) can be distinguished from normal emotional states (eg, grief) and warrant specific treatment. The same understanding helps delineate neurologic conditions (Table 3) requiring different treatments. Such conditions include apathy (29), demoralization (07), disinhibition (41), and pathologic laughing and crying (32).

Table 1. Features of Melancholia and Syndromes Mistaken for Clinical Depression

Melancholia
	• Pathologic mood of unremitting gloom or apprehension • Psychomotor retardation or agitation • Vegetative signs reflecting an exaggerated stress response (eg, anorexia and weight loss, slowed bowel motility, insomnia, loss of libido, altered circadian rhythms) • Cognitive impairment in concentration and working memory
Apathy
	• Diminished goal-directed overt behavior (eg, lack of productivity, effort, initiative) • Diminished goal-directed cognition (eg, lack of interests in hobbies or new experiences, lack of concern for one’s health) • Diminished emotional concomitants of goal-directed behavior (eg, unchanging affect, absence of excitement or emotional intensity) • Not attributable to intellectual impairment, emotional distress, or diminished arousal
Demoralization
	• Nonpathologic, sad, or dysphoric mood in response to illness • Emotional responsivity to positive events • Feelings of understandable helplessness and hopelessness • Feelings of subjective incompetence (eg, “I can’t do it”) • Pessimistic thinking with demanding or indifferent behavior

Table 2. Features of Hypomania and Syndromes Mistaken for Bipolar Disorder

Hypomania
	• Infectious, exaggerated happiness or modest, easy irritability when frustrated • Emotional lability, transient with depressive features • Hyperactivity and pressured speech; increased productivity unless mania emerges • Decreased sleep need • Increased appetitive behaviors (eg, food, sex, drugs) • Psychosis uncommon; some psychosensory features may occur
Disinhibition
	• Behavioral impulsivity and coarsening of personality; loss of social graces • Distractibility and modest hyperactivity, but with reduced productivity • Witzelsucht, but no sustained expansive mood state • No psychosis • No change in sleep need
Delirium (hyperactive type)
	• Acute onset, fluctuating course • Altered level of arousal and alertness (EEG abnormal) • Impulsivity, distractibility, fearfulness, irritability • Multisensory hallucinations and delusions • General medical condition (eg, infection) or intoxication (eg, medication overdose) • Signs of general medical illness (eg, fever)
Pathologic laughing and crying (PLC)
	• Paroxysmal and brief • Emotional expression disconnected from emotional experience (emotions are excessive or socially inappropriate) • Denial of feeling the emotion expressed

Table 3. Disturbances of Emotional Expression in Common Neurologic Disorders

Alzheimer disease (31; 27; 44)
	Apathy (45% to 90%): Develops early and may be a presenting complaint. May be misdiagnosed as depressive illness. May be reported as a personality change.
	Melancholia (15% to 50%): Develops early and may be a presenting complaint. Psychotic features and cognitive complaints are common and increase with dementia burden. Association with Alzheimer disease may be due to both conditions being common and not from a common pathophysiology.
	Pathologic laughing and crying (30% to 40%): Crying episodes are the most common feature, followed by mixed laughing and crying.
	Demoralization (less common): Most depressive syndromes do not reflect psychological reactions to being diagnosed or having dementia.
Parkinson disease (23; 26; 38)
	Apathy (30% to 50%): May precede the onset of motor symptoms by years and may be distinct from depression or dementia.
	Melancholia (30% to 50%): May precede the onset of motor symptoms by years. Patients report less guilt and self-punitive ideation than melancholic persons without Parkinson disease. Motor features (bradykinesia, catatonia) may overlap with parkinsonism. Psychotic features must be distinguished from the hallucinations due to Parkinson disease itself or dopaminergic medications.
	Pathologic laughing and crying (5%): Prevalence is as high as 36% in multiple systems atrophy.
Stroke (06; 43; 39; 25; 21)
	Demoralization: “Catastrophic reaction” reported immediately following a stroke.
	Apathy: Features of anergia, bradykinesia, and indifference towards stroke-related disabilities but no exaggeration of deficits. Apathy is also associated with cardiovascular risk factors aside from stroke.
	Pathologic laughing and crying (10% to 25%): Often co-occurs with poststroke depressive syndromes.
	Melancholia: Emerges some time after the stroke, with peak prevalence at 3 to 6 months. Discerning which among these represent apathy syndromes versus melancholia can be difficult. Association with stroke may be due to both conditions being common and not from a common pathophysiology.
Epilepsy (49; 28)
	Depressive syndromes: Depressive syndromes are most associated with complex partial seizures with temporal or frontal lobe foci. Moods are typically short-lived and characterized by a labile, irritable mood. May be accompanied by panic, psychosensory features, or altered arousal.
	Depression may be interictal (most common), postictal (next most common), ictal, or prodromal.
	Melancholia: Common among persons with epilepsy and often unrecognized, even when severe.
Brain tumors (34)
	Tumor histology does not predict symptoms.
	Depression, apathy, and disinhibition are more common than abnormal perceptions and delusions.
	Frontal lobe tumors may cause characteristic frontal lobe syndromes.
	Right-sided lesions are more associated with disinhibition and elevated mood, and left-sided lesions with depression and apathy.
	Temporal lobe tumors produce emotional disturbances related to seizures.
Traumatic brain injury (42; 35)
	Apathy (45% to 70%): Emerges as an early post-trauma feature and may persist if the injury is substantial or involves the dorsolateral prefrontal cortex.
	Pathologic laughing and crying (5% to 11%)
	Demoralization: Prevalence is unknown.
Huntington disease (24; 03)
	Apathy (40% to 50%): May precede onset of motor symptoms by several years. Does not correlate with CAG repeat length. Associated with degeneration of the caudate nucleus. Predicts ability to complete activities of daily living.
	Demoralization: Thought to be common given the stress of a fatal disease, but the prevalence is unknown. Suicide is a definite risk.
	Melancholia: Rare.
	Disinhibition (10%): Accounts for the high comorbidity of bipolar disorders reported in this population.
Wilson disease (22; 02)
	Disinhibition (50% to 70%): Irritability, aggression, and “incongruous behavior”. The 10-fold increase in prevalence of bipolar disorder among persons with Wilson disease likely reflects the prevalence of disinhibition rather than primary manic-depression.
Multiple sclerosis (15)
	Apathy (50%): Risk factors include lesion volume on MRI (particularly in left frontal regions) and cortical atrophy (particularly left anterior temporal).
	Non-melancholic depression. Non-melancholic depressive syndromes (including demoralization) may be more common in women and are associated with younger age of multiple sclerosis onset and increased disability.
	Pathologic laughing and crying (10% to 20%)
Some neurologic treatments with behavioral side-effects
	Apathy: Associated with dopamine-blocking drugs, SNRIs, and SSRIs.
	Non-melancholic depression: Associated interferon and corticosteroids (for multiple sclerosis) and levetiracetam and topiramate (for epilepsy).
	Suicidality: Suicidality is associated with deep brain stimulation and posteroventral pallidotomy for Parkinson disease and other movement disorders (33).
	Disturbances in motor function. The brain’s motor system is extensive and overlaps with other brain systems mediating emotional expression, appetitive drives, executive functioning, speech and language, and posture and ambulation. Changes in motor functioning can be simple (hemiparesis) or complex (parkinsonism). Changes can be subtle and nonspecific (restlessness suggesting anxiety) or dramatic and diagnostic (postures or stereotypy suggesting catatonia).

Parkinsonism and other basal ganglia signs, cerebellar signs, hyper- or hypoactivity, dyspraxia, abnormal gait, and eye movement abnormalities are familiar indications of neurologic disease and are not discussed here.

Catatonia, like parkinsonism, is a syndrome of motor dysregulation. Its core features are mutism, fluctuating stupor, negativism, posturing, stereotypy, automatic obedience, and echophenomena (Table 4). The number of features or their duration required for diagnosis is not experimentally established, but most patients exhibit four or more signs (17). The course of catatonia may be simple/benign or malignant. Catatonia should be assessed whenever a patient exhibits passive uncooperativeness, postures, muscle rigidity not associated with Parkinson disease, or behavior thought to reflect nonconvulsive fits, “conversion” or malingering, excited or hyperactive delirium, seizure-like behaviors, mutism or odd speech patterns not consistent with aphasia, or any of the classic features in Table 4 (16). An intravenous bolus of 1 to 2 mg of lorazepam (ie, the lorazepam challenge) is a confirmatory test, with modest to significant abatement of features being diagnostic (19).

Catatonia can be missed, first, from the mistaken idea that patients with catatonia must be frozen in an odd posture. Most patients with catatonia speak and move about. Associated mood, speech, and language disturbances and psychotic features may be so intense that clinicians lose full attention to motor signs. Second, catatonia has different presentations, and some manifestations appear willful or feigned (eg, tightly closing lips when being fed, standing when asked to sit, or singing loudly when spoken to). Excited forms of catatonia (eg, manic delirium) are characterized by excessive motor activity, disorientation, and fantastic confabulation. In retarded forms (eg, Kahlbaum syndrome), patients are stuporous (with generalized analgesia and minimal spontaneous movement or speech) but may retain substantial preservation of awareness.

Many conditions elicit catatonia (Table 5), the most common being manic-depression, followed by general medical conditions associated with delirium, seizure disorders, encephalitis, and disease or trauma to frontal lobe circuits. Patients with critical illness and delirium may be at especially high risk (51). Why only some patients with these conditions develop catatonia is unknown (13). Neurologic etiologies should be considered when an older person, without a history of mood disorder, exhibits catatonic features, especially if unilateral or associated with parietal signs (eg, neglect, dyspraxia, or dysgraphia) (01) and when a younger person experiences acute onset of psychotic symptoms or seizure-like episodes (40) or self-injurious tics (12). In patients with seizures, catatonia is typically short (less than 1 hour), recurrent, and accompanied by psychosensory features. Catatonic patients with altered arousal may have partial complex or absence status epilepticus, with foci in the prefrontal and supplementary motor areas, basal ganglia, or anterior temporal lobes (20; 37). In patients with movement disorders, catatonia may be misdiagnosed as “hysteria.” Behaviors thought to reflect motor “conversion” or “psychogenic” movement disorder might be understood as catatonia. Studies confirm that many such patients have ultimately identifiable nervous system pathology (18; 45), the majority of which is associated with right unilateral cerebral lesions and ictal or inter-ictal EEG abnormalities (11) or contralateral frontal and thalamic hypometabolism (05).

Table 4. Features of Catatonia

Observed
	• Stupor • Excitement • Mutism • Stimulus-bound behaviors • Stereotypy • Mannerisms, including speech
Elicited
	• Posturing (catalepsy) • Ambitendency • Waxy flexibility • Automatic obedience (Mitgehen) • Negativism (Gegenhalten) • Stimulus-bound speech

Table 5. Differential Diagnosis of Catatonia

Neurologic conditions
	• Postictal states • Nonconvulsive status • Complex partial seizures • Basal ganglia disease • Stroke (ischemic and hemorrhagic) • Encephalitis • Postencephalitic states • Temporal lobe infarction • Thalamic lesions • Demyelinating disease • Tuberous sclerosis • Narcolepsy
Psychiatric conditions
	• Mania • Melancholia • Drug-induced states (eg, PCP) • Withdrawal states (eg, dopamine agonists, benzodiazepines, disulfiram) • Autism spectrum disorders • Schizophrenia
General medical conditions
	• Metabolic derangements • Infection • Endocrine disorders • Autoimmune disorders • Burns
Conditions mistaken for catatonia
	• Parkinson disease • Obsessive-compulsive disorder • Malignant hyperthermia • Locked-in syndrome • Stiff-person syndrome

Perceptual disturbances. Perceptual disturbances occur in all sensory modalities. They include misinterpretations and distortions of environmental stimuli as well as self-generated hallucinations. Psychosensory phenomena differ from other perceptual disturbances in that they are brief (rarely longer than a minute), intense and paroxysmal, and repetitive. They include self-generated hallucinations as well as changes in sensation (autonomic perturbations, dissociation), emotion (incontinence), and memory (false familiarity and unfamiliarity).

Although non-ill persons experience occasional perceptual disturbances, the presence of frequent or intense aberrations indicates serious neuropsychiatric disease (Table 6). Specific neurologic conditions are more likely when (1) a hallucination occurs without other psychopathology, and the patient recognizes it as a symptom of illness or is not troubled by it; (2) multiple hallucinations in multiple sensory modalities occur; (3) the perceptual disturbances are sudden, brief, or occur at a specific time of day; (4) a musical hallucination occurs; (5) illusions and other perceptual distortions predominate the patient’s experience; (6) recurrent transient visual hallucinations predominate; (7) kaleidoscopic hallucinations of shifting geometric colored patterns or visual fragments occur; (8) the perceptual disturbance occurs with an alteration in arousal or awareness or with repetitive motor features; or (9) the patient has a history of traumatic brain injury, seizure disorder, or migraine.

Table 6. Psychosensory Features and Their Diagnostic Implications

Phenomena	Description	Differential Diagnosis
Hyperesthesia and hypoesthesia	Distortions of stimulus intensity (eg, a dim light appears as glaring)	Mood disorders, drug intoxications, migraine, histrionic personality
Synesthesia	Stimulation of one sensory modality eliciting a perception in a different sensory modality (eg, “seeing a sound”)	LSD intoxication
Dysmegalopsia	Distortions of the size and shape of objects	Seizure disorder, retinal disease, disorders of accommodation and convergence, chronic manic-depression
Color spectrum distortions	Changes in color perception	Neurodegenerative conditions (darker or dampened colors), caffeinism (blue or yellow hues), migraine (gray or faded colors), digitalis toxicity (green hues)
Illusions	False perceptions or misinterpretations of environmental stimuli	Delirium, manic-depression, schizotypal illness
Hypnagogic and hypnopompic hallucinations	Visual or auditory perceptions, not vivid but distinct from dreams, occurring while falling asleep or on waking	Sleep deprivation in non-ill persons, narcolepsy
Extracampine hallucinations	False perception outside the limits of the normal sensory field (eg, hearing plotters in another country)	Seizure disorder, manic-depression, delirium, illicit drug use
Peduncular hallucinations	Visual perceptions of cartoon-like people or animals that are non-threatening	Vascular and white matter lesions in the rostral brainstem or basal ganglia, pulvinar, or medial and posterior thalamic nuclei
Autoscopic hallucinations	Perceptions of one’s own image, often sensed as vague or slightly to one side	Seizure disorder, focal lesions of the parietal-occipital cortex, intoxications
Lilliputian (or Brobdingnagian) hallucinations	Visual perceptions of small (or gigantic) objects or creatures	Delirium, migraine, Lewy body dementia, seizure disorder, schizophrenia
Tactile hallucinations	Perceptions experienced as emanating from inside the body or from the skin	Parietal lobe disease (eg, seizure disorder), psychostimulant use, alcohol withdrawal, panic attacks
Olfactory (or gustatory) hallucinations	Sudden, intense perceptions of smells (or tastes) that are often unpleasant	Seizure disorder, migraine
Phoneme (voices) hallucinations	Hallucinated voices, varying from vague or muffled whispers to sustained or clear voices, perceived as originating from a source external to oneself	Schizophrenia, manic-depression
Musical hallucinations	Perceptions of vivid, often familiar tunes or lyrics	Acquired deafness (most likely), seizure disorder, stroke or tumor (more commonly right-sided lesions), depressive illness, obsessive-compulsive disorder, alcoholism, schizophrenia
From: (47)

Delusions and abnormal thought content. Delusions are fixed false beliefs, the content of which can be mundane or fantastic. The form of the delusional process can be secondary (delusions arising from an abnormal emotional state or that are based on perceptual aberrations or abnormal thinking) or primary (delusions emerging de novo from arbitrary conclusions). No delusional form or content is pathognomonic, and most often, the presence of a delusion reflects illness severity rather than specific pathophysiology. However, certain content or forms of delusions suggest diagnosis and involvement of specific brain areas (Table 7). Isolated delusions occurring without associated psychopathology are most often found in definable neurologic conditions. Misidentification delusions point toward right cerebral hemisphere disease (10). Persecutory delusions occur in neurodegenerative conditions, encephalopathy, and temporal lobe dysfunction. Delusions of passivity are more frequent in schizophrenia than in mood disorder, whereas nihilistic delusions occur more frequently in manic-depression (36).

Table 7. Delusions and Their Diagnostic Implications

Phenomena	Description	Differential Diagnosis
Delusions of persecution
• Isolated and simple	“The nurse is trying to kill me”	Neurodegenerative conditions
• Isolated and elaborate	Eg, a man believed his wife and the government had teamed up in a complicated plot to “render him impotent”	Encephalopathy, temporal lobe dysfunction
• Non-isolated	The patient demonstrates other psychopathology	Mood disorders, schizophrenia
Delusions of misidentification
• Capgras syndrome	A relative or familiar person is believed to be replaced by a similar-looking impostor	More often right-hemisphere lesions from a stroke or seizure focus, traumatic brain injury, neurodegenerative conditions
• Fregoli syndrome	Unfamiliar persons are thought to be well known to the patient and often said to be celebrities
• Doppelganger	The belief that one has a double who carries out independent actions
• Reduplicative paramnesia	A familiar person, place, or object is believed to be duplicated
Delusions of passivity
	Experience of being controlled by an outside force or having another person’s thoughts	Schizophrenia, manic-depression, right-hemisphere lesions
Delusions of poverty
	Beliefs of becoming bankrupt or losing one’s home and belongings	Melancholia
Nihilistic delusions (Cotard syndrome)
	Beliefs of being dead or that one’s body or body parts are deteriorating	Manic-depression (90%), brain tumor, migraine
Delusions of grandiosity
	Inflated self-importance and beliefs of superior accomplishments, bodily perfections, and attention from others	Manic-depression, conditions involving frontal lobe circuitry dysfunction
Erotomania
	Delusional belief that one’s love for another person (sometimes a celebrity) is reciprocated	Neurologic disease (25%; degenerative conditions, HIV, seizure disorder, hemorrhage, traumatic brain injury), schizophrenia (35%), mood disorders (22%)
Delusional jealousy (Othello syndrome)
	Delusional beliefs of infidelity or that one’s spouse has been unfaithful	Alcoholism and disorders of cognitive executive dysfunction, epilepsy, schizophrenia (3%)
Delusional memories (paramnesia)
	False memories derived from illusions in association with intense emotion (eg, the depressed person “remembers” past sins)	Mood disorders, schizophrenia
Déjà vu (jamais vu)
	Experience of false (un)familiarity	Chronic limbic system disease (seizures, manic-depression) or hallucinogen use; neurodegenerative conditions
From: (47)

Cognitive dysfunction. Most behavioral disorders have associated cognitive impairments. An increasingly common clinical challenge is faced when a person over 65 years of age presents with a significant decline in behavioral functioning that could represent either melancholia, likely to respond well to treatments, or the early stages of an irreversible condition like Alzheimer disease. Between ages 65 and 75 years, melancholia is several-fold more likely. Table 8 offers guidance through this diagnostic dilemma. When ambiguity persists, all such patients should at least be offered treatments for melancholia.

Table 8. Distinguishing Depressive Pseudodementia From Alzheimer Disease

Clinical Feature	Depressive Pseudodementia	Alzheimer dementia
Mood	Melancholic	Apathetic, avolitional
Cognition	Bradyphrenia, executive dysfunction, recall deficits, false negative errors, some benefit from serial presentation, less behavioral consistency	Visuospatial deficits, executive dysfunction, recall deficits, false negative errors, no benefit from serial presentation, more behavioral consistency
Insight	Exaggerates problems	Minimizes problems
Course	Episodic; more discrete onset	Progressive; insidious onset with mild cognitive impairment
Personal history	Mood disorder	Late-life nonmelancholic depression
Family history	Mood disorder	Dementia
Functional imaging	Frontal or diffuse hypometabolism	Biparietal and temporal hypometabolism
Structural imaging	Normal or with mild atrophy without progression	Temporal atrophy and ventricular enlargement

Personality and personality change. Personality represents a pattern of behavioral traits that are dimensional (not categorical) and involves a complex interaction between genetic influences and developmental environmental factors. Abnormal personality is a distortion of normality personality traits, developing in similar fashion to other physical attributes and, thus, is not associated with identifiable neuropathology. The maturation process of personality, whether normal or abnormal, mostly occurs during the first 2 decades of life. After that, personality changes very little.

A substantial personality change after the age of 35, therefore, almost always is the result of brain dysfunction. Disease, injury, and toxicity can cause such change by disrupting the neural networks subserving personality and altering trait behavior. Individuals with known neuropsychiatric illness (eg, epilepsy) may develop permanent personality changes after decades of illness (Table 9). Personality changes in persons without known neuropsychiatric illness tend to occur when new onset illness or trauma (eg, tumor, stroke, and basal ganglia disease) affects frontal lobe circuitry, resulting in apathy or disinhibition (14; 48). These personality changes are often observable years before other more defining features of the diagnosis become manifest.

Table 9. Personality Changes Seen in Neuropsychiatric Disease

Descriptor	Behavioral Traits	Differential Diagnosis
“Epileptic”	Adhesive and viscous, stubborn and perseverative, humorless sobriety, pedantic and circumstantial speech, hypergraphic, pseudo-profundity, hyposexual	Epilepsy (up to 60%), chronic manic-depression
“Paranoid”	Moody and irritable, suspicious and defensive, quarrelsome and litigious, “neighborhood crank”	Chronic limbic system disease, alcoholism
“Emotional”	Deep emotions, intense expressions, easily tearful, Witzelsucht, hyperreligious	Epilepsy (less common)
“Frontal lobe”	Lateral orbital prefrontal: irritability and emotional lability, episodic dyscontrol and unplanned violence, suspiciousness, restlessness and impulsivity, self-destructive and lacking insight, childishly self-centered and insensitive, overly talkative Dorsolateral prefrontal: lack of spontaneity and initiative, loss of drive or ambition, loss of interests, sluggish, socially isolative, dysphoric	Stroke (particularly large or multiple lesions in anterior areas), tumor (left frontal areas associated with apathy, right frontal areas with disinhibition), traumatic brain injury (40% lateral orbital prefrontal, 10% to 30% dorsolateral prefrontal, 30% to 50% mixed), neurodegenerative conditions
“Rigid”	Inflexible, stoic, frugal, slow-tempered, orderly, muted emotional expression, vulnerability to depression	Parkinson disease

Prognosis and complications

Behavioral disturbances are substantial factors determining quality of life for persons with neurologic disease. Compared to the general population, suicide risk is increased among patients with Huntington disease (12-fold), epilepsy (11-fold), traumatic brain injury (8-fold), multiple sclerosis (7-fold), stroke (2-fold), and migraine with aura (3-fold) (04).

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Contributors

All contributors' financial relationships have been reviewed and mitigated to ensure that this and every other article is free from commercial bias.

Author

M Justin Coffey MD

Dr. Coffey of the Menninger Clinic and Geisinger receives equity as Chief Medical Officer of Workit Health.
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Editor

Howard S Kirshner MD

Dr. Kirshner of Vanderbilt University School of Medicine has no relevant financial relationships to disclose.
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Former Authors

Amy A Pruitt MD
Michael Alan Taylor MD

ICD & OMIM codes

ICD-10: Episodic mood disorders: F30-F39

Personality and behavioral disorders due to brain disease, damage, and dysfunction: F07

Mental and behavioral disorders due to psychoactive substance abuse: F10-F19
ICD-11: Symptomatic and course presentations for mood episodes in mood disorders: 6A80

Secondary personality change: 6E68

Disorders due to use of unknown or unspecified psychoactive substances: 6C4G

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Neurologic disorders associated with behavioral symptoms

Also Relevant

Depression after stroke
Multiple sclerosis: neurobehavioral aspects
Psychogenic seizures
Psychophysiological vertigo (psychogenic vertigo)
Psychophysiological insomnia

Functional brain system	Psychopathologic features
Frontal lobe circuits	Catatonia, basal ganglia signs, apathy and disinhibition (“frontal lobe syndromes” (Tekin and Cummings 2002))
Cerebellar-pons	Apathy, mutism, disinhibition
Dominant cerebral cortex • Frontal • Temporal • Parietal	Apathy, disinhibition Psychosensory phenomena Gerstmann syndrome (dysgraphia, dyscalculia, finger agnosia, and left-right disorientation)
Non-dominant cerebral cortex • Frontal • Temporal parietal	Motor aprosodia Misidentification delusions; passivity delusions; receptive aprosodia; psychosensory phenomena
Stress response system	Melancholia, anxiety disorders
Hedonistic reward system	Substance abuse
Arousal system	Stupor, delirium, sleep disorders

Neurologic disorders associated with behavioral symptoms …

Neurologic disorders associated with behavioral symptoms

Introduction

Overview

Key points

Clinical manifestations

Presentation and course

Table 1. Features of Melancholia and Syndromes Mistaken for Clinical Depression

Table 2. Features of Hypomania and Syndromes Mistaken for Bipolar Disorder

Table 3. Disturbances of Emotional Expression in Common Neurologic Disorders

Table 4. Features of Catatonia

Table 5. Differential Diagnosis of Catatonia

Table 6. Psychosensory Features and Their Diagnostic Implications

Table 7. Delusions and Their Diagnostic Implications

Table 8. Distinguishing Depressive Pseudodementia From Alzheimer Disease

Table 9. Personality Changes Seen in Neuropsychiatric Disease

Prognosis and complications

Biological basis

Table 10. Functional brain Systems and Their Signature Psychopathology

Differential diagnosis

Management

References

Contributors

Author

Editor

Former Authors

ICD & OMIM codes

This is an article preview.
Start a Free Account
to access the full version.

Questions or Comment?

Also in This Category

Neurogenetics and genetic and genomic testing

Acute traumatic spinal cord injury

Tumors of the skull base

Toxic and nutritional deficiency optic neuropathies

Third nerve palsy

Nystagmus

Brain death/death by neurologic criteria

Outpatient rehabilitation of chronic neurologic conditions

Neurologic disorders associated with behavioral symptoms

Introduction

Overview

Key points

Clinical manifestations

Presentation and course

Table 1. Features of Melancholia and Syndromes Mistaken for Clinical Depression

Table 2. Features of Hypomania and Syndromes Mistaken for Bipolar Disorder

Table 3. Disturbances of Emotional Expression in Common Neurologic Disorders

Table 4. Features of Catatonia

Table 5. Differential Diagnosis of Catatonia

Table 6. Psychosensory Features and Their Diagnostic Implications

Table 7. Delusions and Their Diagnostic Implications

Table 8. Distinguishing Depressive Pseudodementia From Alzheimer Disease

Table 9. Personality Changes Seen in Neuropsychiatric Disease

Prognosis and complications

Biological basis

Table 10. Functional brain Systems and Their Signature Psychopathology

Differential diagnosis

Management

References

Contributors

Author

Editor

Former Authors

ICD & OMIM codes

This is an article preview. Start a Free Account to access the full version.

Questions or Comment?

Also in This Category

Neurogenetics and genetic and genomic testing

Acute traumatic spinal cord injury

Tumors of the skull base

Toxic and nutritional deficiency optic neuropathies

Third nerve palsy

Nystagmus

Brain death/death by neurologic criteria

Outpatient rehabilitation of chronic neurologic conditions

This is an article preview.
Start a Free Account
to access the full version.