Case 22- brain Flashcards
Motor loops- Basal ganglia
- Role of the basal ganglia is to facilitate behaviour and movements and inhibit unwanted or inappropriate movements.
- It is the direct and indirect motor loops which allow or inhibit these movements.
- When a structure of the basal ganglia is compromised there is an inability to switch smoothly between commands that initiate and maintain a movement and those that terminate the movement.
Nuclei of the basal ganglia
- Input nuclei (receive information)- caudate nucleus, Putamen
- Intrinsic nucleus (process the information)- Globus pallidus externus, Subthalamic nucleus, Substantia nigra (pars compacta)
- Output nucleus (sends out information)- Globus pallidus internus, Substantia nigra (pars reticulata)
Direct pathway of the basal ganglia- up to Globus pallidus internus
- Excitatory- allows movement to occur
- Movement is initiated from the cerebral cortex causes excitation of neurones in the striatum (corticostriatal pathway)
- Glutamate is released to the Caudate and Putamen
- Excitation of striatal neurones (striatopallidal or striatonigral neurones) inhibit the activity of the globus pallidus internus and substantia nigra par reticulata through the release of GABA
Direct pathway of the basal ganglia- after globus pallidus internus
- Globus pallidus internus and substantia nigra pars reticulata neurones are inhibitory therefore reducing their action on the thalamus results in increased activity of thalamic neurones due to reduced GABA release
- Increased activity of the thalamic neurones (increased Glutamic acid release) causes excitation of the cells of the cerebral cortex therefore allowing movement to occur
- Dopaminergic neurones of the substantia nigra pars compacta project to the striatum exerting an excitatory influence on the striatal neurones through the release of Dopamine
Direct pathway- Parkinson’s disease
Degeneration and depigmentation of the substantia nigra pars compacta which project to the striatum. This causes akinesia/bradykinesia as it causes underactivity of the direct pathway. As there is decreased inhibition of the Globus Pallidus internus and the Substantia nigra pars reticularis, more inhibitory signals are released so less excitatory signals are released from the thalamus reducing the cortex’s activity.
Indirect pathway of the Basal ganglia up to Globus pallidus internus
- Signals from the cerebral cortex activate (excitatory) neurones in the striatum through the release of Glutamic acid
- Excitation of striatal neurones (striatopallidal) inhibit the activity of the globus pallidus externus through the release of GABA
- This prevents the globus pallidus externus neurones (pallidosubthalamic fibres) from inhibiting the subthalamic nucleus neurones, less GABA is released
- Resulting in the increase of activity of the subthalamic nucleus neurones which leads to the activation of the globus pallidus internus and substantia nigra pars reticulata neurones through the release of Glutamic acid
Indirect pathway of the Basal ganglia after the globus pallidus internus
- The inhibitory globus pallidus internus and substantia nigra pars reticulata inhibit the thalamic neurones from projecting to the cerebral cortex therefore stopping the stimulation of unwanted movement. No release of Glutamic acid from the Thalamus
- Dopaminergic neurones of the substantia nigra pars compacta project to the striatum (nigrostriatal pathway) and can inhibit activity of the indirect pathway. Through the release of Dopamine which is inhibitory
Hyperdirect pathway
The subthalamic nucleus can also receive excitatory signals from the cerebral cortex.
Indirect pathway- Parkinsons disease
- Indirect pathway - dopamine has an inhibitory effect on neurones that project to globus pallidus externus.
- Loss of striatal dopamine causes overactivity of the indirect pathway
- Causes inhibition of the globus pallidus externus neurones, disinhibition of the subthalamic nucleus and therefore excessive excitation of the internal segment of globus pallidus. Reducing activity in the Thalamus and cerebral cortex
- Induced akinesia (loss of power of voluntary movement)
Indirect pathway- Huntington’s disease
- Excessive, unwanted, abnormal movements (dyskinesias) occur in Huntington’s disease.
- Degeneration of the striatum (caudate nucleus and putamen)
- In this condition there is an attrition of cells that project to the external segment of the globus pallidus.
- This leads to disinhibition of the external pallidal neurons and inhibition of the subthalamic nucleus
- The globus pallidus internus neurones therefore become abnormally underactive and involuntary movements (chorea) occur as there is reduced activity in the indirect pathway. So overexcitation of the thalamus and cerebral cortex.
Other disorders of the motor pathway
Abnormal movements occur as a complication of the long-term treatment of Parkinson’s disease with levodopa – causes underactivity of the indirect pathway and overactivity of the direct pathway.
Ballism/Hemiballism/Hemiballismus
- A rare condition caused by damage to the subthalamic nucleus (often by stroke).
- Characterised by gross choreic, flailing movements of the contralateral limbs due to removal of the excitatory drive upon basal ganglia output neurons.
Alzheimer’s disease summary
- Commonest form of dementia- approximately 50-70% of UK cases
- Heterogeneous, caused by ageing along with a complex interaction of genetic and environmental risk factors
- Post mortem shows conglomeration of amyloid plaques and tau neurofibrillary tangles; current hypothesis is that these are degradation products rather than targetable pathology
- Insidious, gradual onset over months and years
- Early memory loss followed by later more complex and varied symptoms e.g. personality change, apraxia, apathy…
- MDT is key- refer to memory clinic! Clinical diagnosis with supporting evidence
- Pharmacological and non-pharmacological approaches should be used in conjunction
- Treatment first line = AChE inhibitors, Second line = Memantine
Vascular dementia summary
- Second most common cause of dementia (10-15%)
- Risk Factors include history of stroke or TIA, AF, hypertension, diabetes, hyperlipidaemia, smoking, obesity, coronary heart disease…
- Family history of stroke or cardiovascular disease
- Presentation varies significantly, as does speed of progression. May be simply cognitive decline, may be features of weakness, visual disturbances, apathy… Depends on area of brain
- Clinically, there is often an overlap with Alzheimer’s disease
Lewy body dementia summary
- Dementia characterised by eosinophilic intracytoplasmic neuronal inclusion bodies (Lewy bodies) in the brainstem and neocortex
- Spectrum of Lewy body disorders, which may overlap, that include Parkinson’s disease and Parkinson’s disease-associated dementia
- Probably third most common cause of dementia in the UK
- Diagnosis of probable LBD requires two of the three core features: Fluctuating attention and concentration, Recurrent well-formed visual hallucinations, Spontaneous Parkinsonism
- DAT scans are useful although not diagnostic- remains a clinical diagnosis
- Avoid antipsychotics- can make Parkinsonism worse
- Treat with AChEs – most evidence is for rivastigmine.
Frontotemporal dementia summary
- This is a progressive dementia, which typically affects the frontal and/or temporal lobes (atrophy)
- Probably 4th most common form of dementia (5%)
- One of the more common causes of dementia before the age of 65
- Features include: Loss of inhibition, Inappropriate social behaviour, Loss of motivation but without depression (apathy vs depression!!), Loss of empathy and sympathy, Change in preferences, Repetitive or compulsive behaviours, rituals, Loss of control over eating or drinking, Difficulties with planning, organisation or decision making.
- Memory and visuospatial skills usually preserved in early stages. Cognitive deficit less apparent than behavioural changes.
- Lack of insight.
- Loss of awareness of personal hygiene, and incontinence as the disease progresses.
- No pharmacological treatment available
Mental capacity
One’s ability to understand the nature of ones actions and to voluntarily enter into a contract
Mental capacity act- 2005
- A person must be assumed to have capacity until proved otherwise
- A person is not to be treated as having a lack of capacity until all practical steps have been taken to try prove otherwise, without success
- An unwise decision does not been someone lacks capacity
- An act done on behalf of someone who lacks capacity must be for their best interest
How to assess mental capacity
Two key assessment points:
- a person lacks capacity if they have an impairment or disturbance in the functioning of the brain
AND is unable to make decisions as they cant:
- understand information
- retain information
- use or weigh the information to make decisions
- communicate the rationale behind their decisions
It is task specific as patients may have capacity to make some but not other decisions
When can informed consent not be obtained
- When patients are incapacitated but need the emergency treatment to save their life
- When patients with severe mental health conditions lack the capacity to consent
- When the patient needs hospitalisation for severe mental health conditions
- When the patient needs an additional emergency procedure during an operation
- When the patient is a risk to public health i.e. TB
- When a patient is severely ill and living in unhygienic conditions
What makes consent valid
- Must be voluntary i.e. made by the person and not influenced
- Informed i.e. the person must know all the information to include benefits and risks, alternatives etc
- Capacity i.e the person must be able to understand the information
How to manage situations when informed consent cant be obtained in adults
- See if there is a valid advance refusal
- See if there is a donee/attorney
- If there is no advanced refusal / attorney then the HCP should determine what the persons best interest would be (past/present wishes, beliefs and values etc) and go ahead with the treatment they believe first this
Attorney/donee
A person appointed by the person who has lost capacity (the donor) to make decisions on their behalf after the loss of capacity.
Independent mental capacity advocate
Someone appointed to speak and act on your behalf if you lack capacity to make certain decisions. This is for those with no friends/family to support and represent them.
What to do when a person who lacks capacity refuses treatment?
Can be legal to detain and treat them under the Mental Health Act 1983
- section 2 = admit for up to 28 days for assessment
- section 3 = admit for up to 6 months for treatment
- section 4 = admit for up to 72 hours in emergencies
The use of restraint
May be appropriate when in a patients best interest i.e. to prevent harm to the person and if this harm is proportionate to the risks of detainment.
Court of protection
Protects those incapacitated by focusing on their best interests:
• Can clarify the validity of advanced refusals
• Can appeal decisions
• Can remove a done
• Can appoint deputees
Capacity in children
- Legally assumed to have capacity from age 16
- Below the age of 16 may be ‘Gillick competent’
- There are still many situations children may lack capacity due to being overwhelmed / coercion / pressure
- The court of protection can overrule treatment refusal if it will lead to their death or severe injury - Mental Capacity Act 2005
Parental responsibility vs competent child wishes
- Parents have the right until the child becomes an adult at 18. Even though children have capacity from 16. This is under the children act 1989
- Refusing treatment that comes from a young person may be overridden by parental wish to give consent on their child’s behalf
- But if a parent refuses their child treatment this can be overruled by the courts if it is in the best interest of the child
Who can consent for children
- Biological mother or father
- Legally appointed guardian
- A person with a residence order concerning the child
- A local authority with an emergency protection order for the child
Role of occupational therapist in dementia
Provide advice on adaptations to the home
Also advise on any equipment that could allow people to maintain their independence for as long as possible
Role of SALT in dementia
Aid communication skills and help with swallowing problems which could affect a persons diet and weight loss
Impact of dementia
Big impact on a person emotionally, socially, psychologically and practically
Can affect memory, senses and emotions, self-esteem, independence lost, relationships
A person may lose the ability to do their favourite activities, hobbies or every day skills
Economic burden to the NHS
High prevalence
Benefits of MDT
Decreases risk of abuse
Improves health outcomes
Smoother care
Helps to build trust and respect between the professionals and patients
Helps to promote patient centred medicine
Reduces duplication of certain services
Role of NHS in dementia care
Diagnosis Clinical care Emotional support Nursing and community support Advocacy Safeguarding Training provision Research End of life care
Challenges the NHS faces in dementia treatment
Ageing population - more complex healthcare
Budget limitations
Service coordination
Numbers of doctors and nurses
Government role in dementia treatment
Service planning and provision Training provision Public health and education Funding Research Budget allocation Legislation Safeguarding
Challenges the government faces in dementia treatment
Ageing population- associated costa
Role of social care in dementia treatment
Care provision Care coordination Carer and family support Advocacy Safeguarding Housing/care homes
Challenges to social care in dementia treatment
Ageing population- increased care needs
Separation of NHS and social care
Limited funding
Role of the family in dementia treatment
Provision of care Emotional support Safeguarding Financial support/planning Power of attorney End of life planning Advocacy Care coordination Nursing care?
Challenges to the family due to dementia
Financial strain
Time commitments - working adults
Emotional strain
Lack of knowledge
