GEP (Life control) Week 6 Flashcards
What is the cerebral cortex, explain what a sulci and gyri, and what hemispheres of the brain do.
It is the region of higer cognitive function, it is the outer later that lies on top of the cerebrum. It consists of grey matter.
Sulci: Depressions in the brain
Gyri: Uplifing in the brain
Hemispheres control and sense contralateral (opposite) side of the body
Temporal region – marks the passage of time, when you go grey/lose hair it can start here
What are the roles of the brain region
What are wernickes, broca and arcuate fasciculum
Wernicke’s area
Posterior superior temporal gyrus* (encompasses auditory cortex)
Responsible forcomprehension of written and spoken language
Damage => fluent but “receptive aphasia”
E.g., w-EAR-nicke’s word salad like “ A salad macaroni doesn’t eat crows”
Broca’s area
Inferior frontal gyrus*
Speech production and articulation
Damage => limited language ”expressive aphasia” single words/v short sentences
Understandable
Arcuate fasciculum
White matter bundle connecting Wernicke’s and Broca’s
Damage here messes with repetition = “conduction aphasia”
Where and what is pre-central gyrus, post-central gyrus and central sulcus
Central sulcus devides the frontal and pariatal lobe
Motor movement occurs in the pre-central gyrus
Sensory: sensation occurs in the post-central gyrus
What is the homunculus analogy
Each hemisphere of the brain generally controls movement and sensation on the opposite side of the body, e.g., contralateral
If an elderly person comes to the hospital confused and lathargic withouth a known cause what do you do
Firstly you need to think of biological pathology, for example like DDxs: UTI, brain injury, stroke, sepsis, diabetes (hypo/hyper), Alzheimer’s, psychosis, blood loss etc etc etc
Tests
-Collateral history (remember confidentiality)
-Examinations e.g., Cranial nerves, motor and sensory
-Bloods (FBC, ESR/CRP, LFTs, U&Es, TFT, B12, folate, glucose (BM – think diabetes), syphilis, HIV and cultures (think SEPSIS)
-Neuroimaging (CT head in 1 hour if suspected injury and 2x vomits)
What are the specific tests for cognition
-Mini Mental State Examination (MMSE): screening, not diagnostic
-Abbreviated Mental Test Score (AMTS): always use on admission if >65 yo in secondary care
Gives a baseline of cognitive ability
<8 should consider memory clinic (links in notes)
-Montreal Cognitive Assessment (MoCA)
-4AT (good for delirium assessment and discussed on the next page!)
How is MMSE classified
Orientation (in time and place)
* Registration (non-related objects)
* Attention and calculation (serial 7s)
* Recall
* Language and copying
Generally:
* 24-30: NORMAL (no cognitive impairment)
* 18-23: mild cognitive impairment
* 0-17: severe cognitive impairment
Specifically for Alzheimer’s:
* ○ 21-27: mild
* ○ 14-20: moderate
* ○ 10-14: moderate
Serial 7 is counting down from 100
What is delirium
Altered level of consciousness (Hyper/Hypo
Disorientation
Inattention
Acute onset*
Differs to dementia which is chronic and often has a slow, insidious onset
- Should be reversible but has a curious time course, e.g., can last for days, weeks, or even a year.
What is the ICD classification of dementia
What is dementia
Dementia is an umbrella term used to describe a range of symptoms associated with cognitive impairment
50-75% Alzheimers
20-30% Vascular
10-25% Lewy Bodies
10-15% Frontotemporal
What are the 7 A’s of Alzheimers
Overview of alzheimers
Risk factors
>65 yo
Female
Down’s syndrome
T21 gene
APOE4
Traumatic brain injury
Symptoms
Getting lost/forgetting (hippocampal atrophy)
Emotional changes (amygdala)
Later on, problems identifying/categorising objects, learning and understanding spoken words (receptive aphasia) (widespread cortical atrophy)
Pathophysiology: Main area it affects is the hippocampus
Neuronal cell death (of cholinergic neurons) by:
-Extracellular plaques (beta amyloid);
-Intracellular neurofibrillary tangles (tau).
**Treatment **
First line (mild/moderate): Increase cholinergic transmission at the synapse with cholinesterase inhibitors (Donepezil/Rivastigmine/Galantamine)
Second line (moderate-severe): NMDA receptor antagonist (Memantine)
beta amyloid (biproduct of normal cellular metabolism)
*Hippocampus: learning, memory formation, long term memory, spatial memory – hence why the getting lost aspect can happen
Alzheimers also impacts:
Temporal neocortex: Difficulty in understanding spoken words (Receptive Aphasia)Disturbance with selective attention to what we see and hear. Difficulty with identification and categorisation of objects. Difficulty learning and retaining new information.
Subcortical nuclei: movement regulation along with the rest of the basal ganglia (BIG ROLE IN PARKINSONS)
Overview of the vascular Dementia
Risk factors
>65 yo (arteries stiffen w/ age) Family history
Hyperlipidaemia
Hypertension
Type II diabetes
Smoking
Symptoms
Slowed thinking
Difficulty making decisions and planning (executive function)
Stepwise decline
Symptoms can be localized to brain region affected – so could be a random range of issues
Why?
Arterial infarcts +/- chronic ischemia cause neuronal death in cortical regions.
Treatment
Addressing risk factors (other dementia drugs won’t work
white matter beneath the cortex. These nerve fibres carry signals between different parts of the cortex, including the frontal lobes. A person with subcortical vascular dementia will therefore often have slowed thinking and problems with executive function.
What is lewy body dementia
*Lewy Body is similar to Parkinson’s… but in Parkinson’s the motor symptoms present first
Risk factors
>60 yo
Family history Male
Parkinson’s
Symptoms
Hallucinations
Rapid Eye Movement (REM) sleep disorder
Apathy/depression
Incontinence
Fluctuating levels of cognitive impairment – problems with understanding, memory and thinking.
Parkinsonism (later stage*): bradykinesia, resting tremor and rigidity
**Pathophysiology **
Misfolded alpha synuclein inclusions e.g., “Lewy Bodies” within neurons. Causes reduction of cholinergic neurons in the substantia nigra, paralimbic and neocortical areas.
**Treatment (same as Alzheimers): **
First line (mild/moderate): Increase cholinergic transmission at the synapse with cholinesterase inhibitors (Donepezil/Rivastigmine (its a patch so easier to use) /Galantamine)
Second line (severe): NMDA receptor antagonist (Memantine)
Presentation: Lewy Body Dementia
- Hallucinations - seeing, hearing or smelling things that
are not there ( One of the main ones) - Rapid Eye Movement (REM) sleep disorder
- Parkinsonism: bradykinesia, resting tremor and
rigidity (One of the main ones) - Fluctuating levels of cognitive impairment - problems
with understanding, memory and thinking (One of the main ones) - Bladder/bowel problems
- Apathy/depression
NB: Symptoms typically occurs before parkinsonism, but usually both features occur
within a year of each other. This is in contrast to Parkinson’s disease, where the
motor symptoms typically present at least one year before cognitive symptoms
-LDOPA is not used used to the hullucinations that can can occur with it
Levodopa is the precursor to dopamine. Most commonly, clinicians use levodopa as a dopamine replacement agent for the treatment of Parkinson disease. It is most effectively used to control bradykinetic symptoms apparent in Parkinson disease.
What is the Diagnosis Pathway for Dementia
How do you approach challanging dementia behaviour
ABC charts:
– Before the defined behaviour (antecedent)
– During the defined behaviour (behaviour)
– After the behaviour had taken place (consequence)
