Disorders of Mental Status


The disorders of mental status include focal syndromes, such as aphasia, apraxia, agnosia, and neglect, followed by more diffuse syndromes, such as delirium and dementia. The aphasias are discussed in Chapter 5.2 .

Apraxia: Neurology of Learned Movement

Apraxia is a disorder of learned motor acts not caused by paralysis, incoordination, sensory deficit, or lack of understanding of the desired movement. In practical terms, apraxia is an inability to carry out skilled motor acts to respond to a command when the patient understands the command and can perform the same motor act in a different context. Liepmann, a German clinician, described three types of apraxia: ideomotor, ideational, and limb kinetic.

It is important to differentiate several diverse motor phenomena that are commonly confused with the principal varieties of apraxia. These are constructional, dressing, oculomotor, and gait apraxia.

Constructional apraxia , characterized by visuospatial difficulties, is associated with right hemispheric lesions. These patients may be unable to copy a drawing of a clock or a house. In most instances, this deficit is related to neglect of the left side of space or failure to appreciate the spatial relations of items rather than to a motor planning deficit, hence apraxia may not be the best name for it.

Dressing apraxia is also associated with right hemisphere lesions. The patients have difficulty relating the spatial aspects of a garment to the body. Again, this is a visuospatial deficit and not a true motor apraxic deficit.

Oculomotor apraxia refers to a difficulty with voluntary direction of the eyes in gaze and is associated with damage to the brainstem mechanism for control of eye movements.

Gait apraxia refers to an inability to walk that is not clearly explained by primary motor weakness, ataxia, or sensory loss. There is no easy way to demonstrate that the same sequential actions can be performed normally in a different context; therefore, it is unclear whether this gait disorder is a true apraxia.

A last example is apraxia of speech , discussed in Chapter 5.2 . Whether apraxia of speech is a true apraxia is debated by aphasia experts.

Ideomotor Apraxia

Ideomotor apraxia refers to the failure to carry out a motor act in response to a verbal command, yet the patient understands the command and has the motor capacity to perform the same action in a different context. By Liepmann’s model, the idea of the movement, decoded in Wernicke area, is disconnected from its execution in the premotor cortex of the frontal lobe. Ideomotor apraxia often accompanies aphasia in patients with left hemisphere lesions. Only a small percentage of patients with ideomotor apraxia have right-sided lesions. Patients with ideomotor aphasia typically fail to carry out the requested action to verbal command and perform only slightly better in imitation of the examiner, but they carry out the act much better when given the actual object.

A lesion in the left temporal lobe, which also causes aphasia, prevents information regarding the desired act from reaching the left premotor area. Ideomotor apraxia may be part of the deficit in Wernicke aphasia, but the impairment of comprehension makes it difficult to ascertain whether the patient has understood the command. In conduction aphasia and Broca aphasia, ideomotor apraxia may interfere with the patient following commands with limbs on either side of the body. Such apraxic deficits may create the mistaken impression that the patient has a comprehension deficit; asking the patient yes or no questions or giving simple pointing commands are tests to establish that auditory comprehension is intact. Finally, lesions of the corpus callosum can prevent motor information from reaching the right hemisphere motor area. This callosal apraxia affects movement of the left limbs only. The existence of callosal apraxia implies that the left hemisphere is dominant not only for speech but also for learned motor acts, because the right hemisphere cannot program the skilled movements independently.

This association of aphasia and apraxia may reflect the underlying symbolic nature of both speech and gestural expression, or it may simply reflect the anatomic contiguity of centers for speech–language function and those for learned motor acts. The association between apraxia and aphasia explains why most patients with aphasia cannot learn complex gestural languages such as American Sign Language.

Ideational Apraxia

Ideational apraxia is a more complex phenomenon than ideomotor apraxia. Heilman proposed the term “conceptual apraxia” as a similar form of apraxia. There are two competing definitions of ideational apraxia. Some authors use it to mean apraxia for real objects. Ochipa and colleagues described a patient who could name objects but not demonstrate their use, as if he had lost the concept of their purpose (apraxia for tool use). The second definition of ideational apraxia is the loss of the ability to carry out a multistep activity, although each individual step may be performed appropriately. For example, a patient may not be able to fill, light, and smoke a pipe or assemble a coffee percolator and make coffee. Failure to carry out a series action may reflect a motor planning difficulty, as seen in frontal lobe lesions. It may be a more sensitive test for apraxia than single motor commands. By either definition, ideational apraxia is associated with left hemisphere lesions, often large temporoparietal lesions associated with severe aphasia. Both ideomotor and ideational apraxia also occur in Alzheimer disease (AD).

Limb-Kinetic Apraxia

The third of Liepmann’s apraxia syndromes is limb-kinetic apraxia, a deficit of fine motor acts involving only one limb. Patients with mild pyramidal tract lesions may not be weak in gross limb movements but may have difficulty with rapid or fine movements of the fingers. Such apraxia may be a sign of a partial corticospinal tract lesion with mild weakness. Heilman and colleagues referred to this type of apraxia as a “loss of deftness.” A left hemisphere lesion may be associated with limb-kinetic apraxia of both hands, whereas a right hemisphere lesion is usually associated with limb-kinetic apraxia of the left hand only.

Agnosias: Neurology of Recognition

Agnosias are disorders of recognition. Most affect a single sensory system (visual, auditory, or tactile agnosia), and others involve specific classes of items within a modality (prosopagnosia which is agnosia for faces and phonagnosia which is agnosia for familiar voices). In each case, the patient must be shown to have normal primary sensory perception, normal ability to name the item once it is recognized, and no general cognitive deterioration or dementia.

For example, a patient with visual agnosia may fail to recognize a bell by sight but can identify and name it by the sound of the bell ringing or by palpating it. Each sensory modality carries a somewhat arbitrary division between primary sensory cortical deficits and agnosia. Most agnosias require bilateral cortical lesions, cutting off input from the sensory modality in both hemispheres to the left hemisphere language centers.

In the visual system, bilateral occipital lesions may cause cortical blindness; partial lesions may permit primary visual perception of the elements of an object or picture, such that the patient can draw lines or angles representing the item but cannot identify the item. Shown a drawing of a pair of glasses, the patient may report two circles and identify it as a bicycle.

Prosopagnosia, or the inability to identify faces, is a subtype of visual agnosia in which patients cannot recognize family members or friends, although they can describe features, such as hair color, a mustache or beard, or accessories (e.g., hats or glasses). Frequently, the patient with prosopagnosia identifies the person by voice or gait pattern. Oliver Sacks described prosopagnosia, or perhaps a more profound visual agnosia, in The Man Who Mistook His Wife for a Hat .

Auditory agnosias also overlap with the syndrome of cortical deafness resulting from bilateral lesions of the temporal cortex. Some patients with bilateral temporal lobe lesions have preserved pure tone hearing but cannot understand spoken language. As discussed in Chapter 5.2 , this deficit is referred to as pure word deafness. Geschwind suggested that pure word deafness results from a bilateral disconnection of the input from the primary auditory cortex (Heschl gyrus) to the left hemisphere Wernicke area. Rarely, patients show preserved auditory comprehension but impaired nonverbal auditory recognition, for example, identification of animal sounds or the characteristic sounds associated with an object such as a bell. This deficit is called auditory nonverbal agnosia. A last bitemporal syndrome is phonagnosia, the inability to recognize familiar voices.

In the tactile modality, parietal lesions often disrupt the identification of objects by feel, a deficit called astereognosis. A related deficit, agraphesthesia, involves the inability to recognize letters or numbers drawn on the hand. If the patient can describe the sensory characteristics of an object but not identify it, this can also qualify as tactile agnosia. In rare instances, patients with bilateral parietal lesions have no ability to recognize objects by touch on either side.

Delirium

No disorder in neurology is more striking or more distressing to patients, families, and medical personnel than delirium or acute encephalopathy. Delirium is second only to stroke as a cause for neurologic consultation Vanderbilt University Medical Center.

Delirium is defined as “a transient disorder of cognition and attention, one accompanied by disturbances of the sleep–wake cycle and psychomotor behavior.” Multiple cognitive functions are affected in disparate areas of the brain.

Delirium typically involves alterations in the following features, although not all of them are seen in all patients or at once:

  • Disturbed level of consciousness

    • Somnolence

    • Hypervigilance

    • Agitation

  • Disturbed perception

    • Hallucinations

    • Illusions

    • Delusions

  • Psychomotor abnormalities

    • Restlessness

    • Agitation

    • Disturbed sleep–wake cycle

  • Autonomic nervous system hyperactivity

    • Tachycardia

    • Hypertension

    • Fever

    • Diaphoresis

    • Tremor

In current usage, the term delirium can be diagnosed when the patient is agitated, in a normal state of alertness, or somnolent.

Delirium is a common neurobehavioral syndrome, occurring in 30% to 50% of hospitalized patients over age 70. Because almost 50% of hospitalized patients are elderly, it is estimated that as many as 10% of hospitalized medical and surgical patients are encephalopathic at any given time. Though delirium often resolves over days to weeks, a substantial proportion of patients have ongoing cognitive deficits.

A number of specific risk factors for delirium have been identified:

  • Preexisting cognitive deficits

  • Age older than 80 years

  • Prior brain disorder

  • Hearing loss

  • Vision loss

  • Fracture on admission

  • Symptomatic infection

  • Stress

  • Environmental changes

  • Medications including

    • Neuroleptics

    • Narcotic analgesics

    • Sedatives

    • Anticholinergic drugs

  • Medical procedures including

    • Use of restraints

    • Bladder catheterization

    • Surgery

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