Cognitive disorders: introduction and оvervier.

Cognition includes memory, language, orientation, praxis,

judgment, conducting interpersonal relationship, and problem solving.
Cognitive disorders not only reflect disruption in one more of the
above domains but are also frequently complicated by behavioral
symptoms. Cognitive disorders exemplify the complex interface
between neurology, medicine, and psychiatry in that medical or
neurological conditions often lead to cognitive disorders that are, in
turn, associated with behavioral symptoms. It can be argued that of all
psychiatric conditions, cognitive disorders best demonstrate how
biological insults result in behavioral symptomatology. The psysician
must carefully assess the history and context of the presentation of
these disorders before arriving at a diagnosis and treatment plan.
Fortunately, advances in molecular biology, diagnostic techniques, and
medication management have significantly improved the ability to
recognize and to treat cognitive disorders.
Althought cognitive disorders may cross-sectionally present
with similar symptoms, this heterogeneous group of illnesses may
significantly differ in their etiologies, courses, and treatments. As a
case in point, delirium and Alzheimer's disease may present with
impaired recall, yet the former condition is episodic and reversible
whereas the latter illness is a neurodegenerative process for which
there are only symptomatic treatments.
Patients often develop or are evaluated for cognitive disorders
in the medical setting and are not evaluated by a psychiatrist unless
there are significant behavioral disturbances that interfere with day-to-
day patient management. The high prevalence of psychiatric symptoms
and syndromes in medically ill patients without prior psychiatric
histories saliently demonstrates the psysician's obligation to anticipate
cognitive complications in the medical or surgical setting. Optimum
treatment for cognitive disorders results from a collaborative effort
between the patient's primary psysician and a psychiatrist.
Delirium is defined by the acute onset of fluctuating cognitive
impairment and a disturbance of consciousness with reduced ability to
attend. There are frequent associated perceptual abnormalities, sleep-
wake cycle disturbances, disorganized thought process, and abnormal
psychomotor activity. A significant public health problem that
forebodes poor outcome, delirium is associated with cognitive and
functional decline, complicates medical courseb and increases resource
use and mortality risk.
Cost of delirium:
1.Increased nursing care
2.Increased lenght of stay
3.Increased risk of cognitive decline
4.Increased risk of functional decline
5.Increased mortality
6.Delay postoperative mobilization
7.Prevention of early rehabilitation
8.Increased rate of nursing home placement
 9.Increased need for home care services
10.Increased distress to caregivers
11.Barrier to psychosocial closure in terminally ill
patient
Delirium is most often caused by multiple etiologies, such as
infections, metabolic abnormalities, endocrinopaties, substance
intoxication, and withdrawal. In line with the many causes of delirium,
there are several theories proposed to explain its pathophysiology.
These include neurochemical abnormalities, inflammatory changes,
oxidative stress, blood-brain barrier dysfunction, and interactions
between these factors. An organized approach to the diagnosis and
management to delirium maximizes the practitioner's effectiveness in
determining and correcting the etiologies and providing safety and
education to patients and caregivers. There is much research to be
done on the basic and clinical aspects of delirium.
Comparative nosology.
Psychiatrists in the United States refer to delirium as the
sindrome of fluctuating attention, cognitive impairment, perceptual
disturbance, and sleep-wake cycle abnormatilies that develop in a
short time period. Neurologists may be more likely to refer to a similar
syndrome as an acute confusional state. Others use the terms
encephalitis or encephalopathy. The multiple terms used to describe
delirium lead to confusion and variable there sholds to make a
diagnosis. This is signification because early recognition of dilirium
may improve prognosis. An important consideration in creating
diagnostic criteria for delirium is that, if the criteria are too stringent,
mild cases of delirium may be left undiagnosed and untreated, despite
being harbingent of poor outcome.
Searching for the etiology of the delirium is an essential step in
the management of the delirious patient. Some nosological systems
refer to the delirium solely based on cause. DSM-IV-TR subdivides
delirium as to whether the causes are a general medical condition,
substance withdrawal, substance intoxication, or multiple etiologies.
Other classifications are more specific about cause but less specific
about defining the delirium. For example, the terms uremic and
hepatic encephalopathy and limbic encephalitis are used in the medical
literature and clinical practice. Encephalophaty is not clearly defined,
and any central nervous system (CNS) disturbance related to uremia or
hepatic pathology may meet the nonspecific diagnostic criteria.
Encephalitis, like encephalopathy, is not well defined and may
represent any CNS change. For example, limbic encephalitis refers to
paraneoplastic syndromes with CNS manifestations. Encephalitis and
encephalopathy lack specificity and potentially include patients with
dementia, coma, or any CNS manifestations of a disease, even if the
patient does not have a delirium.
The many synonyms for delirium often confuse clinicians and
researchers and create barriers to diagnosis and management.
Delirium by Other Names:
Intensive care unit psychosis
Acute confusional state
 Acute brain failure
Encephalitis
Encephalophy
Toxic metobolic state
Central nervous system toxicity
Cinchonism
Paraneoplastic limbic encephalitis
Sundowning
Cerebral insufficiency
Organic brain syndrome
Consistent nosology is expected to improve the ability of
clinicians and researchers to refer to the same syndrome and to
improve the validity and the ability to reneralize research on diagnosis,
factors that influence prosnosis, and treatment response. The term
delirium is emphasized in two of the preffered classification systems:
the DSM-VI-TR and the International Classification of Deseases (ICD).
Compatibility of the DSM-IV and ICD is improving with collaborative
efforts by the American Psychiatric Association and the World Health
Organization.
DSM-IV describes delirium based on signs, symptoms, time
course, and etiology. If the delirium is due to a general medical
condition, the history, physical examination, and laboratory studies are
required to place the causative agent as a general medical condition.
The conditions must be coded on Axis III, including all of the medical
conditions that contribute to the delirium. Delirium due to substance
intoxication or delirium due to substance withdrawal is coded if the
clinical evidence, including laboratory studies, supports a toxicological
syndrome (toxidrome) attributable to one or several substances or to
substances withdrawal symptoms, respectively. Delirium due to
multiple etiologies is the most common clinical scenario in patients
with severe medical comorbidities.
Coding in the ninth edition of the ICD(ICD-9) is similar to
DSM-IV-TR in man respects. The specific general medical conditions
and substance involved in the delirium my be coded with the ICD to a
high lever of specificity. The delirium itself is coded under transient
organic mental disorder as acute delirium or subacute delirium. There
are sections of ICD that describe accidental poisonings, with a high
lever of specificity for the agent. For example, if an accidental overdose
of a pesticide occurred, the clinician could find this under accidental
poisoning of an agricultural agent and then could choose wheather the
pesticide was chlorine, phosphate, or carbamate based. Delirium also
can be classified as senile, presenile, or arteriosclerotic delirium. Drug
withdrawal syndromes and drug-induced delirium are described with
an increased specificity of coding choises when compared to the DSM-
IV-TR.

Risk factors and protective Factors

Factors that predispose patients to delirium
Vision Hypertension Use of bladder
impairment catheter
Medical illnesses Chronic Preoperative
cognitive
(severity and obstructive
impairment
quantity) pulmonary disease
Cognitive Alcohol abuse Functional
impairment limitations
Older than 70 Smoking history History of
years of age delirium
Any iatrogenic Abnormal sodium Abnormal
event level potassium,
sodium, or glucose
test
Use of physical Abnormal glucose Preoperative use
restraints level of
benzodiazepines
Malnutrition Abnormal Preoperative use
bilirubin level of narcotic
analgesics
More than three Blood urea Epidural use
medications added nitrogen to
creatinine ratio >
18
 Risk factors. There are numerous factors that increase a
patient's risk for delirium. These range from extremes of age to the
number of medications taken. For example, pharmacokinetic and
pharmacodynamic changes specific to the young and the old contribute
to the increased risk as in both populations. In one study of elderly
hospitalized patients, the risk of delirium was higher if the patients had
vision impairment, more severe medical illness, cognitive impairment,
or an elevated blood urea nitrogen (BUN) to creatinine ratio. Other
studies of ICU patients suggested that hypertension, abnormal total
bilirubin, smoking history, epidyral use, morphine, and intravenous
(IV) dopamine were associated with delirium.
Medications are another important risk factor for delirium.
The risk increases with the number of medications taken and includes
prescribed, illicit, herbal, and over-the-counter medications. The use of
herbal and over-the-counter preparations is associated with delirium,
often throught interactions with other pharmaceuticals or intrinsic
anticholinergetic properties.
Protective Factors It is clear that good premorbid functioning
before delirium predicts better outcome. Given the significant
morbidity and mortality associated with delirium, interventions that
prevent the occurrence of delirium or that foster early recognition have
a significant impact on improving patient outcome and reduce the cost
of caring for delirious patients. a variety of interventions may improve
outcome and may reduce risk. For example, educational programs that
target clinicians or placement of liaison psychiatrists on orthopedic
units improved coordination of care between consultants and primary
care providers. Most studies demonstrated benefit in terms of
decreased frequensy or shorter duration of delirium and decreased
lenght of stay compared to the usual care. Other interventions that
have been studied and that demonstrate benefit include a focus on
nutrition, increased rehabilitation, and attention to visual and hearing
impairment.
Not all interventions have demonstrated benefit. For example
a randomized study of general medical patients older than 65 years of
age compared the usual care to care by a geneatric consultant and a
protocol for systematized rewiew of patient's records. The groups,
followed for as long as 8 weeks, did not differ in time to improvement
from the delirium, and less than one-half of the patients in both groups
demonstrated an increase in Mini-Mental State Examination (MMSE)
of at least 2 point. Additionally, there were no differences between the
groups in measures of delirium severity, lenght of stay, discharge rate
to the community, living arrangements after discharge, or survival.
Future interventional studies are needed to inform the debate about
the content, duration, and method of education programs that may
modify the frequensy, duration, and severity of delirium in various
patient cohorts.
 Hypotheses about delirium pathophysiology
Decreased oxidative Abnormal second messenger
metabolism that uses neurotransmitter as
Reduced cholinergic function first messenger
Dopamine excess Change in blood-brain
Norepinephrine excess barrier permeability
Glutamate excess Endocrine abnormality (e.g.,
Serotonin imbalance hypothalamic-pituitary-
γ-Aminobutyric acid adrenal axis and thyroid
imbalance hormone)
Decreased beta endorphin Decreased somatostatin-like
Abnormal signal reactivity
transduction Inflammatory hypothesis
with cytokine increase

Clinical features
Patients with delirium fluctuate in their ability to focus, to
shift, and to sustain attention; are easily distractible; and demonstrate
impaired memory. Associated symptoms include affective lability,
psychomotor abnormalities, and misinterpretations and
hallucinations. Affective symptoms often fluctuate and may include
anxiety, fear, apathy, anger, euphoria, dysphoria, and irritability, all
within short time periods. The perceptual disturbances are mostly
visual, but they also occur in the other sensory realms. These
perceptual disturbances are often disturbing to the patients and have
been described as poorly organized, fragmented dreams or nightmares.
Confusion and reactivity to hallycinations and disorientation may
dominate the behavioral manifestations of delirium. Patients may
attempt to remove IV lines, catheters, EGG leads, and other tubes or
may attempt to ambulate under unsafe conditions (e.g.,
postoperatively).
Delirious patients are categorized on the basis of alertness and
psychomotor activity. The hyperactive subtype is psychomotorically
active, hypervigilant, restless, and excitable and speaks with loud or
pressured speech. The hypoactive subtype is psychomotorically
slowed, quiet, and withdrawn and has reduced alertness and decreased
speech production. The loud patient gains the attention of others and is
more likely to be diagnosed with delirium than the quiet patient who is
not disturbing other patients or staff. Because delirium carries an
increased risk of morbidity and mortality, the quietly delirious patient
needs to be edentified and appropriatelly evaluated and treated. A
concern with the loud , hyperactive, delirious patient is the increased
use of chemical or mechanical restraints that may carry the risk of
neglecting the appropriate diagnostic evaluation and possibly
worsening the delirium throught polypharmacy.
Although increased motor activity is described as a feature in
some accounts of delirium due to hyperthyroidism, anticholinergetic
toxicity, and alcohol withdrawal, with reliability of motor activity as an
aid in differential diagnosis of delirium is not consistent. Motor activity
in delirium is not consistently associated with etiology, EGG findings,
cerebral blood flow, or ratings of fluctuation.