Session Five (Amnesic Disorders) Flashcards

1
Q

How can we divide memory disorders?

A

By permanence (temporary or permanent) or by cause (neurological or psychogenic).

However there is some overlap, as with Alzheimer’s

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2
Q

What are some examples of neurological memory disorders?

A
  • Toxic confusional state
  • Mild memory disorder following head injury
  • Amnesic syndrome
  • Epilepsy
  • Dementia
  • Cerebral hypoxia
  • TGA
  • Transient Epileptic Amnesia (TEA)
  • HIV neurocognitive disorder
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3
Q

What are some examples of psychogenic memory disorders?

A
  • PTSD
  • Fugue states
  • Focal retrograde amnesia
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4
Q

Briefly outline the different forms of memory? Which are affected in Amnesia?

A
  • Primary (working memory; Memories of the last few seconds
  • Autobiographical memory; Recollection of past incidents and events
  • Semantic memory; Knowledge of language, concepts, facts.
  • Implicit memory; Skills

Autobiographical memory is severely affected in amnesia, semantic memory may be, other two are usually preserved.

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5
Q

Distinguish Antegrade and Retrograde Amnesia?

A

AA = Impairment in new learning i.e in recall and recognition for episodes and facts arising after the onset of illness or injury.

RA = Loss of memory for episodes or facts which occurred before the onset of illness or injury

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6
Q

What are some causes of Transient Neurological Amnesia (loss of memory, neuro cause, temporary)?

A
  • Delirium or Acute Confusional state
  • Head Injury
  • Epilepsy
  • Alcoholic blackout
  • Cerebral hypoglycaemia
  • Transient Global Amnesia
  • Transient Epileptic Amnesia
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7
Q

What is Transient Global Amnesia? What are some suggested causes for it?

A
  • Neuro disorder, characterised by a disruption to almost all memory lasting 2-8 hours
  • Patient only aware of very short term memory and perhaps some very old memories form childhood
  • No other cognitive deficits
  • Cause unclear, dominant theories include cerebral ischaemia, migraines or small epileptic attacks (although most EEGs come back normal)
  • NO link between TGA and vascular diseases like stroke and CVD.
  • Many patient shave history of migraine
  • Some patients will go on to develop de novo epilepsy after TGA episodes.
  • 1/3 cases have a precipitating event, including regroups exercise, sex, cold water swimming, stress, or medical procedures.
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8
Q

What is Transient Epileptic Amnesia?

A
  • Rare neuro disorder
  • Recurring episodes of amnesia caused by underlying temporal lobe epilepsy
  • Both RA and AA, although self recognition is preserved.
  • Other cognitive functions normally preserved, may be a small episode of unresponsiveness
  • 3/4 cases occur during then night with the patient walking up confused
  • Cases that hit when awake are normally preceded by smell/taste hallucinations
  • Diagnosis is often complicated, most patients have negative EEG findings on initial presentation
  • Most are diagnosed at a later date due to the recurring nature of the condition (12+ a year)
  • Most patients are men above the age of 50
  • Over 50% display repeated questioning behaviour
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9
Q

What is “The Amnesic Syndrome” and what can cause it?

A

An abnormal mental state in which memory and learning are affected out of all proportion to other cognitive functions in an otherwise alert and responsive patient.

Form of Persistent Neurological Amnesia

Causes:

  • Post-encephalitis (e.g. herpes)
  • Hypoxia (e.g. from anaesthesia)
  • Thiamine deficiency (e.g. in Korsakoff)
  • TB Meningitis
  • Temporal lobectomy
  • Lesions in specific parts of the brain, namely the medial temporal lobes.
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10
Q

Lesions in which parts of the brain can lead to Antegrade Amnesia?

A
  • MEDIAL TEMPORAL LOBES (most common by far)
  • Thalamus
  • Mammillary bodies
  • Retrosplenium
  • Basal forebrain
  • Frontal lobes
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11
Q

How can Herpes lead to Amnesia?

A
  • 50% first infection
  • 50% reactivation brought on by stress/trauma/sunlight…
  • Travels along olfactory nerve or via dura to the base of the brain
  • From there into the temporal lobes
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12
Q

Outline the neuropsychological features of Amnesic Syndrome

A
  • IQ intact
  • Primary short term working memory intact
  • Severe impairment of explicit memory
  • Extensive autobiographical retrograde amnesia
  • BUT older semantic memories remain spared
  • Procedural skills intact but lack the explicit memories around them e.g. won’t remember they’ve ever played piano but will be able to play is masterfully
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13
Q

What are some common causes of cerebral hypoxia?

A
  • Heroin overdoses
  • Suicide attempts
  • Cardiac arrests
  • Surgical anaesthetic accidents
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14
Q

How strong is the link between cerebral hypoxia and amnesia, and why?

A

20% of cases of CH show memory problems, in absence of other cognitive issues.

Hypoxia causes cell loss across the brain, but about 19% of patients show damage in the hippocampi alone, which is an area associated with memory. Suggestion is that hypoxia can in some people specifically affect this region and cause amnesia.

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15
Q

What are Wernicke’s and Korsakoff’s?

A

Neurological syndromes resulting from profound thiamine depletion, usually caused by alcohol withdrawal.

Technically two different syndromes (K = memory, W = CANON, not memory) but often co-occur in Alcoholic Wernicke-Korsakoff syndrome.

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16
Q

What are the symptoms of Wernicke’s?

A
  • Ophthalmoplegia
  • Nystagmus
  • Ataxia
  • Confusion
    +/- Peripheral Neuropathy
DD = Delirium tremens
Mx = High doses of IV thiamine
17
Q

What are the symptoms of Korsakoff’s syndrome?

A

Severe deficits in memory and learning out of all proportions to other cognitive functions in an otherwise healthy and responsive treatment.

Can however present as a coma, or following W, or insidiously.

18
Q

What brain changes can be seen in a person with W-K syndrome?

A
  • Loss of neutrons, gliosis, micro-haemorrhages in the peri-ventricular and para-aqueductal regions
  • Damage to anterior thalamus, mammilary bodies, mammillo-thalamic tracts
  • Cortical atrophy
  • Loss of large neurons superior frontal cortex, hypothalamus, cerebellum
  • Prefrontal white matter
19
Q

What have studies into the brains of individuals with Antegrade Amnesia shown? And therefore what regions of the brain are likely responsible?

A
  • Most recent and best evidence points to the anterior thalamus, mamillo-thalamic tract.
  • Herpes patients see drop in hippocampal volume
  • K patients show damage predominantly in the thalamus and mammillary bodies, but also hippocampus
20
Q

What theories exist to explain why retrograde amnesia predominantly affects more recent memories?

A
  • Consolidation theory; Over time there is a consolidation/ structural reallocation of memories to the point where they become independent of the hippocampus/ med temp lobes, and therefore are spared from the amnesic effects of damage to this area.
  • Semanticisation theory; Over time episodic memories acquire a more semantic form, and since amnesia predominantly affects episodic memories this may spare them from damage.
  • Multiple trace theory; The hippocampi/ med temp lobes are always involved in the storage, retrieval and reactivation of episodic memories, it’s just that older memories have a greater number of traces laid down for them therefore are less likely to be lost due to damage.
21
Q

What is the “temporal gradient” of retrograde amnesia?

A

The observed phenomenon that amnesia spares relatively early memories but tends to damage more recent ones. True of autobiographical memory and to an extent semantic memory as well.

22
Q

What region of the brain may be responsible for retrograde amnesia? What evidence is there to support this?

A

Frontal lobe atrophy may cause the superimposed retrieval deficit that causes retrograde amnesia.

Evidence:

  • ‘Frontal’ test scores are low in 64% of RA patients
  • RA patients may have reduced brain volume in the frontal, thalamic and med temp regions (MRI)
23
Q

Briefly, what are the dominant hypothesis about the causality of RA and AA?

A

Mamillo-thalamic pathology leads to an acquisition or consolidation deficit, leading to AA

Frontal lobe atrophy leads to a superimposed retrieval deficit, leading to RA.

24
Q

What is Semantic Dementia?

A
  • A variant of fronto-temporal dementia in which we see profound semantic memory impairment (i.e. in naming, word-finding and comprehension)
  • In the context of otherwise normal cognitive function (i.e. well orientated in time and place, intact VS abilities, number skills, reasoning and problem solving, executive skills)
  • Caused by disproportionate temporal lobe atrophy of various aetiologies
  • Usually left-sided or bilateral
  • Commonly misdiagnosed
  • Aka Progressive fluent aphasia
25
Q

Individuals with semantic dementia show poor remote autobiographical memory as well, why might this be?

A
  • May be an issue with autobiographical memory itself

OR

  • May be a consequence of their language and semantic problems.
  • SD is associated with significant comprehension and word finding deficits, which may make it difficult for them to understand the question and then retrieve the correct words to express themselves.
26
Q

What research has been done into the cause of autobiographical memory deficit in Semantic Dementia?

A
  • 3 patients with SD were given memory challenge tests.
  • First with general cues, then with lexical-semantic cues that would help them find the words necessary without actually providing them with the memory
  • Found that they performed a lot better in the second condition, suggesting that once this lexical/language barrier is overcome their autobiographical memory is still functioning.
  • Confirms the belief that SD primarily affects semantic memory.
27
Q

What conditions can lead to semantic memory disfunction?

A
  • Alzheimer’s
  • Vascular dementia
  • Lewy body disease
  • FT dementia
  • CJ disease
  • Huntington’s
  • Dementia in HIV
  • Voltage gated K channel encephalopathy
  • Pseudo-dementias (e.g. depression)