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PSYN824 week 3 2011. Learning outcomes Understand importance of cranial nerve I for clinical neuropsychology practice Be able to identify structures on the dorsal and ventral brain stem and their involvement in common and uncommon brain disorders

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psyn824 week 3 2011

PSYN824 week 3 2011

Learning outcomes

Understand importance of cranial nerve I for clinical neuropsychology practice

Be able to identify structures on the dorsal and ventral brain stem and their involvement in common and uncommon brain disorders

Describe the anatomy of the thalamus and the roles of the major nuclei

Identify the structures that comprise the basal ganglia

Describe the neuropsychology and neuropathology of Parkinson’s disease, Huntington’s disease

Explain how disorders in basal ganglia circuitry produce hypo- and hyper-kinetic movements

the cranial nerves
The cranial nerves

Twelve pairs

  • labelled by Roman numerals, in a rostrocaudal sequence
  • Only the first two (Cranial nerves I and II) enter the CNS in the forebrain

Three functions:

  • provide the sensory and motor information for the skin and muscles of the head and neck
  • convey to the cns the information from key sensory systems: vision, hearing, olfaction and taste

3. important components of the autonomic nervous system, important in visceral functions such as breathing, heart rate and blood pressure

Cranial nerve 1 and neuropsychology

  • Can be damaged via cribiform plate leading to anosmia (olfactory loss)
  • Anosmia associated with frontal tumors, Alzheimer’s and possibly Parkinson’s disease
  • Olfactory nerves → olfactory bulb → olfactory tract → olfactory processing areas (broadly speaking the uncus, entorhinal and the peri- amygdaloid cortex)
  • Projectionds both ipsilaterally and contralaterally processing
brain stem
Brain stem

Brain stem:

  • dorsal aspect: inferior and superior colliculi, cerebellar peduncles and floor of fourth ventricle
  • ventral aspect: optic tract, mammillary bodies (and mammillo-thalamic tract) , infundibulum of hypothalamus (and pituitary stalk), cerebral peduncles, pons, pyramids, olives
  • not visible on surface : reticular formation (including the raphe n and locus coerulus) and the substantia nigra
what is the role of the mammillary bodies mb in memory
What is the role of the mammillary bodies (MB) in memory ?

Paired structure on brain stem

Part of hypothalamus

Integral part of limbic system

Projects to anterior thalamus via mammillothalamic tract; principal input from hippocampus via post-commisural fornix

Implicated in memory by patients with Wernicke-Korsakoff’s syndrome, single case and case series

Kim et al (2009) report that left-sided only functional connectivity between MB and anterior thalamus significantly correlated with delayed verbal recall scores

Diencephalon: thalamus, hypothalamus, and mammillary bodies

Thalamus: two halves are separated on the midline by the third ventricle but joined across the midline band of white tissue called the massa intermedia,

landmark is the internal medullary lamina, a Y shaped sheet of white matter, it divides the grey matter into anterior, medial and lateral sections, contains the intralaminar n; also midline nuclei

Intralaminar nuclei lesions are associated with cognitive deficits and typical “frontal like” behaviour

Pulvinar: Wernicke’s aphasia

Dorsomedial nucleus: anterograde amnesia

Anterior thalamus/mammillary body: anterograde amnesia/frontal signs

Lateral and medial geniculate nuclei are in the optic and auditory pathways

Ventroposteromedial n and ventral posterolateral n involved in allodynia, parathesias

Reticular nuclei: schizophrenia ?

Persistent vegetative state ?

persistent vegetative state
Persistent vegetative state

Description not a prediction

50% reduction in cortical metabolism, which sometimes decreases over time

No visual tracking, but orienting response, sleep wake cycle

poor outcome predicted by: damage to thalamic (bilateral) diffuse regions of cortex, and to white matter regions

May resolve to minimal state of consciousness


Owen et al (2006) reported a case where a 23 yo woman in VS for five month after TBI was able to “willfully modulate” her brain

  • Asked to imagine playing tennis (thinking of the ball volleying back and forth over the net) or walking through her own home, imaging what she could see
  • Increased activity in supplementary motor area (SMA), and parahippocampal gyrus (PPA), posterior parietal lobe (PPC) and lateral premotor cortex (PMC), respectively
from http www9 biostr washington edu da html

Note the relationship between caudate and putamen,

motor disorders linked to basal ganglia aka extrapyramidal system
motor disorders linked to basal ganglia (aka “extrapyramidal” system)
  • diminished movements like in Parkinson’s disease
  • hyperkinetic disorders like Huntington’s disease, Tourette’s and ballism
  • motor stereotypies such as Leigh-Nyham syndrome (self mutilations)
  • OCD incl punding (of course, OCD is not a pure motor disorder)
parkinson s disease paralysis agitans or shaking palsy clinical triad of
Parkinson’s disease (paralysis agitans or shaking palsy) clinical triad of

Parkinson’s disease (PD) is a progressive degenerative disorder which affects about 1% of the population over 65;

The classical clinical motor triad is

  • bradykinesia and akinesia including “iron mask” of PD
  • muscular rigidity, in particular cogwheel rigidity
  • resting tremor

Pathological hall marks

  • progressive loss of the dopaminergic neurons in the darkly pigmented substantia nigra pars compacta
  • presence of intraneuronal inclusions in the cell bodies called Lewy bodies in PD with dementia
hoehn and yahr staging of parkinson s disease
Hoehn and Yahr Staging of Parkinson’s disease
  • Stage One: unilateral disease, minimal functional impairment
  • Stage Two: bilateral disease, without impairment of balance
  • Stage Three: mild to moderate bilateral disease, some postural instability, physically independent
  • Stage Four: severe disability, still able to walk or stand unassisted but markedly physically incapacitated
  • Stage Five: wheelchair bound or bedridden unless aided
non motor impairment in parkinson s disease
Non-motor impairment in Parkinson’s disease

1. Cognitive impairment is independently associated with depression, sleep disturbance and anxiety

  • Depression 25%
  • Dementia 29%, lifetime risk 80%

(Riedel et al 2010)

  • MCI present 19% at diagnosis

Aarsland et al (2009)

As a whole, the data show that, compared to demographic peers, in PD without dementia there are impairments in

  • Attention and executive function
  • Memory
  • Visuospatial functions
  • Language

Presence of bradyphrenia

2. Disorders of impulse control


Abbreviations: SSC, somatosensory cortex; PMC, primary motor cortex; PreMotor, Premotor cortex; PFC, prefrontal cortex; PPC, posterior parietal cortex; DLPFC, dorsolateral prefrontal cortex; GPe, globus pallidus external; GPi, globus pallidus internal; MD, mediodorsal nucleus of the thalamus; VA, ventral anterior nucleus of the thalamus; VL, ventrolateral nucleus of the thalamus, SNr, substantia nigra pars reticulata; SNc, substantia nigra pars compacta; OFC, orbitofrontal cortexTable modified from from Blumenfeld 2010

huntington s disease
Huntington’s disease
  • Inherited, neurodegenerative disease, autosomal dominant disorder, abnormal gene on chromosome 4 mapped in 1983
  • Affects approximately 5-10/100,000
  • Presents with triad of symptoms: motor, cognitive, psychiatric (independent)
  • Average age at onset 30-40 years
  • Average duration of disease onset until death 10-17 years

Sprengelmeyer et al (1996) reported that in preclinical patients there was impaired recognition of facial expression of disgust

  • Problems with replication ?
  • Substantial heterogeneity in clinical presentation
  • Volume of the anterior insula ?
chiccetti et al 2011 brain 134 641 652
Chiccetti et al (2011) Brain 134; 641–652

Figure 3 Cell implants performed in patients with Huntington’s disease and evaluated 18 months following transplantation showed good survival of the grafted neurons, despite the presence of some microglial activation surrounding the grafted areas. Cell implants evaluated 10 years after transplantation showed significant microglial activation specifically in striatal zones of the grafts, which also received cortical glutamatergic connections.

movement disorders
Movement disorders
  • Relative pattern of activity in direct and indirect pathways determines movement
  • Direct pathway “starts” movements
  • Indirect pathways involved in “stopping” and “switches between” movements
  • Neurons in the Gpi have high intrinsic rate of firing, need to be silenced to start movement, activated to stop movement