Neuropsychology

Question 1

What happens to the brain when damaged?

Answer 1

Stop dreaming?
Stop dreaming in images?
Dream more & more vividly?
Nightmares increase?

Does the place of damage affect theories of dreaming?

Scattered accounts in the scientific literature

Question 2

Solms (1997)- systematic review, new data collection

METHOD

Answer 2

434 patient systematically observed

361 patients from whom data could be collected

Matched control group

13 clinical interview questions

Brain damaged recorded

Question 3

Solms (1997)- RESULTS

Answer 3

40 patients with paralysis
- 38 reportes their sensory motor deficits vanished in their dreams

10 blind patients & some aphasia patients
- could speak normally & understand speech in their dreams

Question 4

Theoretical issue- dreaming after brain stem damage

Answer 4

In 18 cases the damage was restricted to medulla/pons/midbrain/hypothalamus & thalamus

Damage anywhere in the brain stem does not lead to loss of dreaming

Question 5

Theoretical issue- loss of visual dreaming

Answer 5

Charcot-Wilbrand syndrome

Loss of ability to conjure up visual images or memories along with the loss of dreaming

2 patients only

Both with damage to medial occipital-temporal region

Question 6

Types

Answer 6

Loss of visual dreaming
Excessive dreaming or dreamlike thinking
Nightmares
Global loss of dreaming

Question 7

Excessive dreaming or dream like thinking

Answer 7

Confused mental state in which dreams frequently confused with reality

Cingulate gyrus involved

Damage is to areas which are close

• medial frontal cortex
• medio-dorsal thalamus
• basal forebrain nuclei

Question 8

Solms interpretation (very speculative) of this frontal medial inferior area

Answer 8

In normal dreaming-
- Abstract ideas formed in pre-frontal cortex
- medial area translates them into concrete form by back projection
- concrete form occurs in association sensory cortex
— this area also may inhibit primary sensory areas to allow the back projection to dominate
— May inhibit motor systems
— May form attention to the concrete form
- in normal waking the medial areas are inhibited & regulated
- excessive dreaming follows when the inhibition is released

Question 9

Nightmares

Answer 9

9 has recurring nightmares

5/9 has epilepsy

As Dream’s become more recurring & more unpleasant, the link to seizure increases

Question 10

Solms interpretation of nightmares

Answer 10

REM or epileptiform discharge or other sources will activate the dream process via an arousal mechanism

This may be the curiosity-interest-expectancy circuits of the ventro-mesial forebrain

• Cell groups situated in the mesolimbic & mesocortical dopamine systems are stimulated
• the system ascends through the forebrain bundles of the lateral hypothalamus, through basal forebrain areas
• descending components of the emotive system probably arise from the latter brain areas

Question 11

Global cessation of dreaming- frontal

Answer 11

9 patients all has damage to white matter anterior to the frontal horns

No memory problems

25% of patients who stopped dreaming had aphasia, this was no different from those without aphasia

The loss of the ability to generate language does not lead to loss of ability to generate dreams

Dreamers & non dreamers did differ on perseveration, disinhibition & adynamia

Question 12

Perseveration

Answer 12

Moto perseveration- if the patient is asked to draw a shape, easily begins to do so but cannot stop at right time & goes on repeating the movement over & over again

Question 13

Disinhibition

Answer 13

A lack of learned adaptive & social constraints on impulsive behaviours & affective displays

Solmes measure it as impulsive responses during word recall, meaning of thematic pictures, arithmetical operations

But really the affective behaviour is a clinical observation

Question 14

Adynamia

Answer 14

Lack of spontaneity & voluntary action

Impoverishment of spontaneous speech, reduction of conversational replies often limited to passive responses to direct questions

Solms uses the word fluency test & clinical observation

Question 15

Global cessation of dreaming: frontal

Answer 15

What has been damaged very similar to that ‘cut’ in frontal leucotomy

In this context it has been extensively considered

Pathways between mediobasal frontal cortex & brainstem & limbic nuclei

The curiosity interest expectancy command systems of the brain which instigate goal-seeking behaviours & an organisms appetitive interactions with the world are therefore implicated in the normal dream process

Question 16

Global cessation of dreaming: parietal cortex

Answer 16

45 of 47 had definite parietal lesions- lateral surface of the inferior parietal lobe

Poorly understood why this is

Speculation is this is critical for creation of 3D representation on perceptual-motor experience

Without it dreams can not be created

Question 17

Solms conclusión regarding frontal damage

Answer 17

Concludes that the loss of interactive interest in the world may be the cause of cessation of dreaming

These circuited are implicated in the instigation of dreams

Parietals areas in the representation of dreams

Question 18

Where damage does not change dreaming

Answer 18

Left pre-frontal convexity= had normal dreaming

15 cases (dorsolateral pre-frontal área)

Suggests that this area has no role in the dream process