Memory Disorders in Clinical Practice

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Memory Disorders in Clinical Practice
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• The best-known amnestic syndrome is Korsakoffs
  syndrome. This syndrome is usually secondary to
  Wernickes encephalopathy, which is due to
  thiamine deficiency. The latter presents with
  various abnormal eye reflexes, ataxia, peripheral
  neuropathy, and clouding of consciousness. After
  recovery from the acute state, the patient may be
  left with severe anterograde memory disturbance,
  confabulation, lack of insight, and a mood
  disturbance. These patients have intact STM.

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• In anterograde amnesia, the holding and acquiring
  memory processes are impaired and patients
  perform poorly on tests of short-term memory. In
  most patients with amnesia, the anterograde
  component is more severe and disabling.
• In retrograde amnesia, patients are unable to
  recall events occurring before the brain insult.
  Retrograde amnesia usually accompanies
  anterograde amnesia, but is often mild and
  affects memory for specific time periods of days,
  weeks, months or several years.

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• The oldest memories are the most resistant to
  dissolution. This temporal gradient, in which
  childhood memories are relatively preserved, is
  most often seen in cases with bilateral temporal
  lesions, Korsakoff syndrome and mild Alzheimers
  disease.
• In contrast, retrograde amnesia, in patients with
  Huntingtons and moderate-to-severe Alzheimers
  diseases does not show as much of a temporal
  gradient.

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Amnesias without Cognitive Impairment

• Severe anterograde amnesia with variable
  retrograde amnesia, episodic memory most
  impaired. Procedural and semantic memory more
  preserved.
• Amnesics retain some memory ability as can learn
  new procedures but show dissociation between
  explicit and implicit memory will have no
  awareness of such learning but will show evidence
  of improvement on some tasks trial after trial

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Amnesias without Cognitive Impairment

• Encephalitis
• Specific damage to hippocampus, dorsomedial
  nucleus of thalamus, mammillary bodies
• Will have spared memories from predamage as shown
  in behavior but have no conscious recollection of
  such memories

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Explicit Vs. Implicit Memory

• Explicit memory is said to be memory dependent on
  conscious recollection of experiences. You can
  state aloud or in writing what you just read,
  heard or experienced, sometimes called
  declarative memory
• Implicit memory involves learning that cannot be
  verbalized, change in behavior without any
  conscious awareness, the learning of habits,
  classical conditioning, procedural learning

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Transient global amnesia is a benign disorder,
but it must be distinguished from other causes of
temporary amnesia
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• Transient global amnesia occurs in middle-aged
  and elderly adults, with such presenting symptoms
  as confusion, anxiety, mild-to-moderate agitation
  and amnesia. The patient typically repeats
  questions concerning location (Where am I?,
  How did I get here?), objects in the
  environment (Whose car is that?), and time.
  Episodes begin abruptly and usually last from two
  to four hours, although the duration can range
  from 30 minutes to 24 hours. During the attack,
  patients retain personal identity and can recall
  remote memories, but are unable to store or
  retrieve newly acquired information.

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• Thus, when patients are told the location and
  date, they will often repeat the question a
  minute later having remembered neither the
  previous question nor the answer. During the
  attack, performance of complex motor tasks is
  preserved the patient may skillfully drive a
  car, dress or throw a ball.

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• After the attack of TGA has resolved, patients
  often have retrograde amnesia spanning minutes to
  hours, during which they cannot recall events
  before the episodes onset. Patients also often
  experience anterograde amnesia lasting hours, in
  which they store and retrieve information in
  short-term memory, but are unable to recall it
  the following day.

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• In many cases, attacks follow specific
  precipitating factors. The most common
  precipitants (in order of decreasing frequency)
  are physical exertion, sexual intercourse,
  emotional stress, physical symptoms (e.g. pain,
  nausea, vomiting), exposure to cold temperatures
  and mild head trauma. The causation of TGA is
  unknown if a precipitating factor can be
  identified, then migraine or other vasospasm my
  be likely

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• The chief disturbance in psychogenic amnesia is a
  sudden inability to recall important personal
  information that is too pervasive to be explained
  by ordinary forgetfulness. In psychogenic
  amnesia, this memory loss is not due to organic
  causes, as in alcoholic blackout and epilepsy, or
  to multiple personality disorder (American
  Psychiatric Association, 1994). Psychogenic
  memory loss is usually the result of an emotional
  trauma.

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• In organic amnesia, personal identity and
  memories (e.g. mothers name, home address) are
  usually preserved, and memory loss follows a
  temporal gradient, in which recently acquired
  memories are more severely affected than older
  memories (Russell and Nathan, 1932). Psychogenic
  amnesia, however, is organized primarily along
  affective, rather than temporal, dimensions
  (Schacter, 1982). Patients with psychogenic
  amnesia characteristically have normal
  acquisition of new information. They can
  remember physicians names and faces and what
  they had for breakfast yesterday. Among
  retrograde memories, however, there are striking
  dissociations. For example, a patient may
  remember more about an American presidents life
  than her own.

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Brain Disorders   1.dementia
Progressive deterioration of various mental
processes including memory, abstract thinking,
concentration, language, social occupational
functioning, self-care and judgment. the
deterioration tends to occur in an approximately
opposite manner in which it is learned
developmentally (e.g., feeding is one of the last
skills to deteriorate).   The prevalence of
dementia increases with age. It is relatively
uncommon before age 60. It occurs in about 1 of
people 65 to 75 4 in 75 to 85 year olds and
over 10 in persons over 85 (this is probably an
underestimate). About twice as many women as men
have dementia, but this may be simply because
women live longer.  
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Although changes in memory or cognition may
accompany normal aging, significant impairment
and disability are not a part of normal aging.  
Some causes of dementia can be treated
effectively to eliminate or greatly improve
cognitive performance. Among older persons,
depression and interactions from multiple
medications are two common and highly treatable
causes of dementia symptoms.  
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Etiology  Alzheimer's Disease (Dementia of the
Alzheimer's Type or DAT). This accounts for about
50 of the cases of dementia. Similar to a
learning disability, this is a diagnosis of
exclusion (e.g., all other possible causes for
the symptoms are ruled out). As yet, we do not
have definitive or totally reliable methods of
diagnosis while the person is still alive
(although a number of methods are in the works).
After death, the diagnosis is confirmed by
autopsy of the brain. At this point, much of the
cerebral cortex has atrophied as many brain
neurons have died. Numerous plaques and tangles
are present throughout the cerebral cortex and
hippocampus (cerebellum and spinal cord are less
effected). DAT is nonreversible.  
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DAT seems to involve a reduction of acetylcholine
(or its transmission). Other possible causes are
an abnormality in chromosome 21 (e.g., as Downs
Syndrome), or other chromosomes (1, 14, 19) an
impairment in our immune system (for example,
AIDS produces a condition that is similar to DAT
in the later stages) or an increase deposit of
aluminum or zinc on the brain (still
controversial). Like other disorders, it probably
has more than one cause and there are probably
many different types of DAT.
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• Dementia caused by Alzheimers disease
• Cognitive abulia
• Brain deterioration
• Abnormal protein plaques
• Holes in neuron cell bodies
• Neurofibrillary tangling
• Significant cerebral atrophy in temporal and
  frontal lobes from loss of neurons

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Other causes of dementia a) Multi-infarct
dementia. this is responsible for about 20 of
the cases. It involves a large number of small
stokes eventually leading to dementia. b)
infections such as herpes, Creutzfeld-Jacob
disease (human variation of "mad-cow" disease by
the way, meat-eaters seem to be twice as likely
to develop dementia than vegetarians), or AIDS.
c) neurological disorders such as Huntington's
Chorea, Parkinson's Disease (not all cases), ALS
(not all cases). d) Vitamin deficiency (often
seen in alcoholics). e) chronic alcohol use
(e.g., Korsakoff Syndrome) f) Pick's Disease
(frontal lobe dementia) g) brain injuries or
cancer.
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• Cortical Dementia
• Dementia of the Alzheimers type
• Fronto-temporal dementia
• Fronto-temporal dementia (frontal-variant)
• Primary Progressive Aphasia
• Semantic dementia
• Fronto-temporal dementia with motor neuron
  disease, or amytrophic lateral sclerosis
• Lewy Body Dementia
• Subcorical Dementia
• Progressive supranuclear palsy
• Huntingtons disease
• Parkinsons disease
• Multiple sclerosis
• Cortico-basal degeneration

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Treatment There is currently no cure for
Alzheimer's or most forms of dementia. Many new
drugs are in the development stage and several
have recently been approved for DAT. Cognex
(Tacrine) is used to treat the symptoms of mild
to moderate Alzheimer's disease. Tacrine will not
cure Alzheimer's disease, and it will not stop
the disease from getting worse. However, tacrine
can improve thinking ability in some patients
with Alzheimer's disease, for a short time
window.. In Alzheimer's disease, many chemical
changes take place in the brain. One of the
earliest and biggest changes is that there is
less of a chemical messenger called acetylcholine
(ACh). Tacrine slows the breakdown of ACh, so it
can build up and have a greater effect. However,
as Alzheimer's disease gets worse, there will be
less and less ACh, so tacrine may not work as
well. Another agent to treat DAT is donepezil
which also slows the breakdown of ACh.
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Treatment for Dementia

• Drugs that increase acetylcholine levels
• tacrine (Cognex) donepezil (Aricept)
• Vitamin E
• Estrogen-replacement therapy (ERT)
• preliminary evidence suggest estrogen may improve
  memory and other cognitive capacities

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DSM Criteria for Delirium

• Disturbance of consciousness, such as reduced
  clarity of awareness of the environment, with
  reduced ability to focus, sustain, or shift
  attention
• Change in cognition or development of a
  perceptual disturbance that is not accounted for
  by a dementia
• Disturbance develops over a short period of time,
  usually hours to days, and tends to fluctuate
  during the course if the day
• Evidence that the disturbance is caused by the
  direct physiological consequences of a medical
  condition

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DeliriumDelirium is characterized by
disorientation, recent memory loss, and clouding
of consciousness
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Delirium

• sudden onset of difficulty concentrating,
  focusing attention, maintaining direct stream of
  thought
• insomnia and/or agitation
• incoherent speech

• disorientation with regard to time, place, person
  
• perceptual disturbance (delusional, paranoid)

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Causes of Delirium

• Alcohol
• Amphetamines
• Anesthetics
• Analgesics
• Antiasthmatic agents
• Anticholinesterase agents
• Anticonvulsants, antihistamines
• Antihypertensive and cardiovascular medications
• Cannabis
• Carbon dioxide, or monoxide
• Cocaine, hallucinogens, opioids
• Corticosteroids
• Muscle relaxants

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Causes of Delirium

• Surgery is often a common underlying cause for
  delirium
• drug intoxication, drug withdrawal reactions
• Other causes include
• metabolic nutritional imbalances, infection or
  fever, neurological disorders, stress
• Elderly persons with dementia are the most
  susceptible to delirium
• age-related physical decline
• vulnerability to stress and disease
• often many prescribed medications

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Treatment of Delirium

• Treatment is generally to identify and treat the
  underlying causal factor.
• Complete recovery is not unexpected
• younger patients recover more quickly

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Dysmnesic States

• In dysmnesic states, memory is not so much lost
  as it is distorted. These conditions are usually
  associated with a diagnosis of some underlying
  neurological impairment or schizophrenia. The
  delusional misidentification syndromes include
  the Capgras syndrome and the Fregoli syndrome.
  In the former, the patient insists that a person,
  usually a close relative or friend, has been
  replaced by an imposter.

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• In the Fregoli syndrome, the patient falsely
  identifies a familiar person, often a persecutor,
  in strangers. There is good evidence linking
  misidentification syndromes to the dysfunction of
  the right hemisphere and to frontal lobe
  disorders.
• Reduplicative paramnesia is a related syndrome in
  which a patient is certain that a familiar place,
  person, object, or body part has been duplicated.
  It commonly presents when a patient insists that
  a familiar place (e.g. his or her hospital room)
  exists in an impossible location (e.g. his or her
  house).

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Delusional Misidentification Syndromes

• Capgrass syndrome or delusion
• Fregolis syndrome or delusion
• Autoscopic delusion

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Capgrass Syndrome

• Considered an atypical psychosis
• A firm belief that family, friends or others have
  been replaced by impersonating doubles
• Less often, pets or personal items replaced by
  imposters or copies
• Brain damage disconnecting memory systems or
  complex visual recognition systems

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Capgrass Syndrome

• Illusion des Soises Illusion of the doubles
• Last known case of witch burning in Europe 1887,
  man killed and burned wife, insisting she wasnt
  his wife but a changeling
• Described in 1923 by Capgras, female patient who
  insisted her husband had been replaced by
  multiple doubles
• More common in women than men
• Does respond to antipsychotics

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Capgrass Syndrome

• Capgrass syndrome may be related to prosoagnosia
• Capgrass has been associated with head injury,
  temporal lobe epilepsy, vitamin B12 deficiency,
  hepatic encephalopathy and diabetes.
• Neuroimaging suggests that frontal lobe pathology
  is involved.

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Capgrass Syndrome

• Pets have been seen as replaced by duplicates
  with the wrong bark or the wrong fur.
• Personal items such as shoes replaced by a more
  worn pair, toothbrush replaced by one with fewer
  bristles, coin collection coins replaced by cheap
  replicas.

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Fregolis Syndrome

• The firm belief that individuals in the
  environment are periodically replaced by
  persecuting imposters. The persecutor changes
  faces, being the mailman one day and a nurse
  another.
• Delusions of persecution in which the same
  perscutor is repeatedly identified as being
  different individuals
• Complete strangers or more often acquaintances
  are accused of being the persecutor.

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Autoscopic Delusion

• Firm belief that one or more doubles of oneself
  exist. Distinct from autoscopic hallucinations
  which occurs in non-psychotic individuals.
• Ones double is seen wearing exact same clothes
  and jewelry, imitating your every action and
  facial gesture.
• Ones image in the mirror is another you. The
  double may be teased, accosted or struck. The
  double is unable to dodge the blows but also
  gives them right back