Chapter 1. Disorders Of Cognitive Function

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Dysarthria, a disorder of articulation, is sometimes difficult to distinguish from aphasia, but it always

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spares oral and written language comprehension and written expression

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Transcortical aphasias are conditions in which

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Transcortical aphasias are conditions in which Wernicke area, the arcuate fasciculus, and Broca area are themselves preserved, but their connections to other parts of the brain are interrupted . . .These disconnection syndromes may be distinguished clinically by the fact that, since the circuit comprising Wernicke area, the arcuate fasciculus, and Broca area is intact, repetition is preserved

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subjective and emotionally charged memories are affected more than retention of objective facts and events

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psychogenic amnesia

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Recent memory¾

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Tests of recent memory assess the ability to learn new material. Typically, the patient is given three or four items to remember and asked to recall them 3 minutes later

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Remote memory

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The practical distinction between recent and remote memory is that only recent memory requires an ongoing ability to learn new information. Remote memory is tested by asking the patient to recall material that someone of comparable cultural and educational background can be assumed to know. Common examples are personal, historic, or geographic data, but the questions selected must be appropriate for the patient, and personal items must be verifiable

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The patient cannot identify, by touch, an object placed in the hand

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Astereognosis

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Astereognosis

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The patient cannot identify, by touch, an object placed in the hand

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The patient cannot identify, by touch, an object placed in the hand

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Astereognosis

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Astereognosis

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The patient cannot identify, by touch, an object placed in the hand

Front 10

This is misplaced localization of a tactile stimulus

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Allesthesia¾

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Allesthesia¾

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This is misplaced localization of a tactile stimulus

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This is misplaced localization of a tactile stimulus

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Allesthesia¾

Front 13

Apraxia is the inability to

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the inability to perform previously learned tasks, such as finger snapping or clapping the hands together, despite intact motor and sensory function. Unilateral apraxias are commonly caused by contralateral premotor frontal cortex lesions. Bilateral apraxias, such as gait apraxia, may be seen with bifrontal or diffuse cerebral lesions.

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Apraxia is the inability to

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the inability to perform previously learned tasks, such as finger snapping or clapping the hands together, despite intact motor and sensory function. Unilateral apraxias are commonly caused by contralateral premotor frontal cortex lesions. Bilateral apraxias, such as gait apraxia, may be seen with bifrontal or diffuse cerebral lesions.

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Unilateral apraxias are commonly caused by

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caused by contralateral premotor frontal cortex lesions. Bilateral apraxias, such as gait apraxia, may be seen with bifrontal or diffuse cerebral lesions

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Unilateral apraxias are commonly caused by

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caused by contralateral premotor frontal cortex lesions. Bilateral apraxias, such as gait apraxia, may be seen with bifrontal or diffuse cerebral lesions

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In the confused patient, pupillary constriction

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suggests opiate ingestion

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In the confused patient, pupillary constriction suggests opiate ingestion; dilated pupils are characteristic of

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anticholinergic intoxication but may also be a manifestation of generalized sympathetic hyperactivity

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the confused patient, pupillary constriction suggests opiate ingestion; dilated pupils are characteristic of anticholinergic intoxication but may also be a manifestation of generalized sympathetic hyperactivity. Small, irregular pupils that react poorly to light, but better to accommodation

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can be seen in neurosyphilis.

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Sedative drugs and Wernicke encephalopathy produce

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nystagmus or ophthalmoplegia. Selective impairment of vertical gaze (especially downward) occurs early in progressive supranuclear palsy

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Sedative drugs and Wernicke encephalopathy produce

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nystagmus or ophthalmoplegia. Selective impairment of vertical gaze (especially downward) occurs early in progressive supranuclear palsy

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Sedative drugs and Wernicke encephalopathy produce

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nystagmus or ophthalmoplegia. Selective impairment of vertical gaze (especially downward) occurs early in progressive supranuclear palsy

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Pseudobulbar Palsy

This syndrome is characterized by

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dysarthria, dysphagia, hyperactive jaw jerk and gag reflexes, and uncontrollable laughing or crying unrelated to emotional state (pseudobulbar affect). It results from bilateral interruption of the corticobulbar and corticospinal tracts. Dementing processes that produce this syndrome include progressive supranuclear palsy and vascular dementia.

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Pseudobulbar Palsy

This syndrome is characterized by

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dysarthria, dysphagia, hyperactive jaw jerk and gag reflexes, and uncontrollable laughing or crying unrelated to emotional state (pseudobulbar affect). It results from bilateral interruption of the corticobulbar and corticospinal tracts. Dementing processes that produce this syndrome include progressive supranuclear palsy and vascular dementia.

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dysarthria, dysphagia, hyperactive jaw jerk and gag reflexes, and uncontrollable laughing or crying unrelated to emotional state (pseudobulbar affect). It results from bilateral interruption of the corticobulbar and corticospinal tracts. Dementing processes that produce this syndrome include progressive supranuclear palsy and vascular dementia.

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Pseudobulbar Palsy

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dysarthria, dysphagia, hyperactive jaw jerk and gag reflexes, and uncontrollable laughing or crying unrelated to emotional state (pseudobulbar affect). It results from bilateral interruption of the corticobulbar and corticospinal tracts. Dementing processes that produce this syndrome include progressive supranuclear palsy and vascular dementia.

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Pseudobulbar Palsy

Front 27

Myoclonus, which consists of rapid shocklike muscle contractions, can occur with

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uremia, cerebral hypoxia, or hyperosmolar nonketotic states.

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Myoclonus, which consists of rapid shocklike muscle contractions, can occur with

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uremia, cerebral hypoxia, or hyperosmolar nonketotic states.

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Myoclonus, which consists of rapid shocklike muscle contractions, can occur with

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uremia, cerebral hypoxia, or hyperosmolar nonketotic states.

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Dementia
Myoclonus
Motor signs are useful in the differential diagnosis of dementia

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Creutzfeldt-Jakob disease, HIV-associated dementia

Front 31

Dementia
Myoclonus
Motor signs are useful in the differential diagnosis of dementia

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Creutzfeldt-Jakob disease, HIV-associated dementia

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Dementia with ataxia DD

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Spinocerebellar degenerations, Wilson disease, paraneoplastic syndromes, Creutzfeldt-Jakob disease, HIV-associated dementia.

Front 33

Dementias associated with prominent sensory abnormalities and loss of tendon reflexes include

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vitamin B12 deficiency, neurosyphilis, and HIV-associated dementia.

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plantar grasp reflex consists of

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flexion and adduction of the toes in response to stimulation of the sole of the foot

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plantar grasp reflex consists of

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flexion and adduction of the toes in response to stimulation of the sole of the foot

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plantar grasp reflex consists of

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flexion and adduction of the toes in response to stimulation of the sole of the foot

Front 37

palmomental reflex is elicited by

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is elicited by scratching along the length of the palm of the hand and results in contraction of ipsilateral chin (mentalis) and perioral (orbicularis oris) muscle

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palmomental reflex is elicited by

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is elicited by scratching along the length of the palm of the hand and results in contraction of ipsilateral chin (mentalis) and perioral (orbicularis oris) muscle

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is elicited by scratching along the length of the palm of the hand and results in contraction of ipsilateral chin (mentalis) and perioral (orbicularis oris) muscle

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palmomental reflex

Front 40

is elicited by scratching along the length of the palm of the hand and results in contraction of ipsilateral chin (mentalis) and perioral (orbicularis oris) muscle

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palmomental reflex

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Delirium Tremens - Tx

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Treatment consists of diazepam, 10-20 mg intravenously, repeated every 5 minutes as needed until the patient is calm, and correction of fluid and electrolyte abnormalities and hypoglycemia. The total requirement for diazepam may exceed 100 mg/h. Concomitant b-adrenergic receptor blockade with atenolol, 50-100 mg/d, also has been

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Delirium Tremens - Tx

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Treatment consists of diazepam, 10-20 mg intravenously, repeated every 5 minutes as needed until the patient is calm, and correction of fluid and electrolyte abnormalities and hypoglycemia. The total requirement for diazepam may exceed 100 mg/h. Concomitant b-adrenergic receptor blockade with atenolol, 50-100 mg/d, also has been

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Delirium Tremens - Tx

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Treatment consists of diazepam, 10-20 mg intravenously, repeated every 5 minutes as needed until the patient is calm, and correction of fluid and electrolyte abnormalities and hypoglycemia. The total requirement for diazepam may exceed 100 mg/h. Concomitant b-adrenergic receptor blockade with atenolol, 50-100 mg/d, also has been

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classic signs of sedative drug overdose are

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confusional state or coma, respiratory depression, hypotension, hypothermia, reactive pupils, nystagmus or absence of ocular movements, ataxia, dysarthria, and hyporeflexia

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classic signs of sedative drug overdose are

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confusional state or coma, respiratory depression, hypotension, hypothermia, reactive pupils, nystagmus or absence of ocular movements, ataxia, dysarthria, and hyporeflexia

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Sedative drug withdrawal is treated with

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Sedative drug withdrawal is treated with a long-acting barbiturate such as phenobarbital, administered orally to maintain a calm state without signs of intoxication, and tapered over about 2 weeks

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Sedative drug withdrawal is treated with

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Sedative drug withdrawal is treated with a long-acting barbiturate such as phenobarbital, administered orally to maintain a calm state without signs of intoxication, and tapered over about 2 weeks

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Sedative drug withdrawal is treated with

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Sedative drug withdrawal is treated with a long-acting barbiturate such as phenobarbital, administered orally to maintain a calm state without signs of intoxication, and tapered over about 2 weeks

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Phencyclidine (PCP) Tx

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Benzodiazepines may be useful for sedation and treating muscle spasms, and antihypertensives, anticonvulsants, and dantrolene (for malignant hyperthermia) may be required. Symptoms and signs usually resolve within 24 hours.

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Phencyclidine (PCP) Tx

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Benzodiazepines may be useful for sedation and treating muscle spasms, and antihypertensives, anticonvulsants, and dantrolene (for malignant hyperthermia) may be required. Symptoms and signs usually resolve within 24 hours.

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Phencyclidine (PCP) Tx

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Benzodiazepines may be useful for sedation and treating muscle spasms, and antihypertensives, anticonvulsants, and dantrolene (for malignant hyperthermia) may be required. Symptoms and signs usually resolve within 24 hours.

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50 mL of 50% dextrose intravenously, should be begun immediately

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HYPOGLYCEMIA

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50 mL of 50% dextrose intravenously, should be begun immediately

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HYPOGLYCEMIA

Front 54

Two hyperglycemic syndromes

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diabetic ketoacidosis and hyperosmolar nonketotic hyperglycemia

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Two hyperglycemic syndromes

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diabetic ketoacidosis and hyperosmolar nonketotic hyperglycemia

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HYPOADRENALISM
tx

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Treatment is administration of hydrocortisone and correction of hypovolemia, hypoglycemia, electrolyte disturbances, and precipitating illnesses.

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HYPOADRENALISM
tx

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Treatment is administration of hydrocortisone and correction of hypovolemia, hypoglycemia, electrolyte disturbances, and precipitating illnesses.

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HYPOADRENALISM
tx

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Treatment is administration of hydrocortisone and correction of hypovolemia, hypoglycemia, electrolyte disturbances, and precipitating illnesses.

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Hyponatremia, particularly when acute, causes

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causes brain swelling

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Hyponatremia, particularly when acute, causes

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causes brain swelling

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Hyponatremia, particularly when acute, causes

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causes brain swelling

Front 62

Hyponatremia, particularly when acute, causes

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causes brain swelling

Front 63

Excessively rapid correction of hyponatremia may cause central pontine myelinolysis, a disorder of white matter that can produce

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confusional state, paraparesis or quadriparesis, dysarthria, dysphagia, hyper- or hyporeflexia, and extensor plantar responses. Severe cases can result in the locked-in syndrome (see Chapter 10), coma, or death

Front 64

HYPERCALCEMIA


Symptoms include

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thirst, polyuria, constipation, nausea and vomiting, abdominal pain, anorexia, and flank pain from nephrolithiasis. Neurologic symptoms are always present with serum calcium levels higher than 17 mg/dL

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HYPERCALCEMIA dx

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shortened QT interval on the ECG.

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HYPERCALCEMIA dx

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shortened QT interval on the ECG.

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HYPERCALCEMIA dx

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shortened QT interval on the ECG.

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HYPERCALCEMIA dx

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shortened QT interval on the ECG.

Front 69

WERNICKE ENCEPHALOPATHY
Pathologic features include

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euronal loss, demyelination, and gliosis in periventricular gray matter. Proliferation of small blood vessels and petechial hemorrhages may be seen. The areas most commonly involved are the medial thalamus, mammillary bodies, periaqueductal gray matter, cerebellar vermis, oculomotor, abducens, and vestibular nuclei.

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WERNICKE ENCEPHALOPATHY
Pathologic features include

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euronal loss, demyelination, and gliosis in periventricular gray matter. Proliferation of small blood vessels and petechial hemorrhages may be seen. The areas most commonly involved are the medial thalamus, mammillary bodies, periaqueductal gray matter, cerebellar vermis, oculomotor, abducens, and vestibular nuclei.

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WERNICKE ENCEPHALOPATHY
Pathologic features include

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euronal loss, demyelination, and gliosis in periventricular gray matter. Proliferation of small blood vessels and petechial hemorrhages may be seen. The areas most commonly involved are the medial thalamus, mammillary bodies, periaqueductal gray matter, cerebellar vermis, oculomotor, abducens, and vestibular nuclei.

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WERNICKE ENCEPHALOPATHY
Pathologic features include

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euronal loss, demyelination, and gliosis in periventricular gray matter. Proliferation of small blood vessels and petechial hemorrhages may be seen. The areas most commonly involved are the medial thalamus, mammillary bodies, periaqueductal gray matter, cerebellar vermis, oculomotor, abducens, and vestibular nuclei.

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WERNICKE ENCEPHALOPATHY
classic syndrome comprises the triad of

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ophthalmoplegia, ataxia, and confusional state.

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WERNICKE ENCEPHALOPATHY
classic syndrome comprises the triad of

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ophthalmoplegia, ataxia, and confusional state.

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WERNICKE ENCEPHALOPATHY
classic syndrome comprises the triad of

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ophthalmoplegia, ataxia, and confusional state.

Front 76

WERNICKE ENCEPHALOPATHY
classic syndrome comprises the triad of

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ophthalmoplegia, ataxia, and confusional state.

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WERNICKE ENCEPHALOPATHY
classic syndrome comprises the triad of

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ophthalmoplegia, ataxia, and confusional state.

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WERNICKE ENCEPHALOPATHY
Tx

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Treatment requires prompt administration of thiamine. An initial dose of 100 mg is given intravenously, before or with dextrose, to avoid precipitating or exacerbating the disorder.

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WERNICKE ENCEPHALOPATHY
Tx

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Treatment requires prompt administration of thiamine. An initial dose of 100 mg is given intravenously, before or with dextrose, to avoid precipitating or exacerbating the disorder.

Front 80

WERNICKE ENCEPHALOPATHY
Tx

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Treatment requires prompt administration of thiamine. An initial dose of 100 mg is given intravenously, before or with dextrose, to avoid precipitating or exacerbating the disorder.

Front 81

WERNICKE ENCEPHALOPATHY
Tx

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Treatment requires prompt administration of thiamine. An initial dose of 100 mg is given intravenously, before or with dextrose, to avoid precipitating or exacerbating the disorder.

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WERNICKE ENCEPHALOPATHY
prognosis

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Horizontal nystagmus and ataxia, however, resolve completely in only about 40% of cases. The major long-term complication of Wernicke encephalopathy is Korsakoff syndrome.

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ENCEPHALOPATHY
prognosis

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Horizontal nystagmus and ataxia, however, resolve completely in only about 40% of cases. The major long-term complication of Wernicke encephalopathy is Korsakoff syndrome.

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ENCEPHALOPATHY
prognosis

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Horizontal nystagmus and ataxia, however, resolve completely in only about 40% of cases. The major long-term complication of Wernicke encephalopathy is Korsakoff syndrome.