Topic 3 Neurological Conditions Flashcards
What are neurotransmitters?
Chemicals which allow the transmission of signals from one neuron to the next across synapses
What does dopamine do?
Critical for memory and motor skills
What does GABA do?
Mood modulator - When transmitters are too low these neurons can become excited leading to anxiety and irritability
What does glutamate do?
Major mediator of excitatory signals
What does serotonin do?
Inhibitor - imbalance is related to depression and sleep disorders
What does ACH do?
Excitatory - critical for sleep, attentiveness
What does norepinephrine do?
Flight or fight response
What does epinephrine do?
Abnormal levels linked to sleep disorders/anxiety
What is neurotransmission?
process by which neurotransmitters are released by the axon terminal of a neuron, bind to and activate the receptors on the dendrites of another neuron
Steps of neurotransmission
1 - action potential arrives at the axon terminal.
2 - calcium channels open and calcium enters the axon terminal
3 - increase in calcium causes the synaptic vesicles to move to the presynaptic membrane.
4 - neurotransmitter is released using exocytosis.
5 - neurotransmitter diffuses across the synapse and binds with receptors on the postsynaptic neuron
Define delirium
Acute transient confusional state of altered LOC, hallucinations and restlessness
Onset of delirium
Rapid (2-3 days)
What are the symptoms of delirium?
slurred speech altered LOC hallucinations restlessness tremor distress conversation incoherent violent inattentiveness misperception and misinterpretation
What are the risk factors of delirium?
older age dementia severe illness alcoholism co-morbidities vision impairment hearing impairment history of delirium
What are the consequences of delirium?
prolonged hospitalisation functional decline increased use of restraints increased mortality possible development of dementia within two years need for long term nursing home care
Define dementia
Umbrella term for several diseases characterised by progressive cognitive impairment and brain dysfunction not caused by impaired LOC
Onset of dementia
Gradual
Symptoms of dementia
Loss of memory, intellect, rationality, social skills, physical functioning, orientation and language
Alterations in behaviour and normal functioning Personality changes Mood swings Difficulty recognising family Manner flat Aggressive Decline in ability to perform ADLS
Agnosia Apraxia Dysphasia Expressive dysphasia Receptive dysphasia
Define alzheimers
Devastating condition characterised by progressive memory loss, impaired thinking, neuropsychiatric symptoms, inability to perform routine ADLs and intellectual deterioration interfering with social or occupational function
Stages of alzheimers
Mild: apparent in hindsight. Apathetic, lose interest in hobbies, less willing to try new things and adapt, slower to grasp complex ideas
Moderate: problems are more apparent and disabling. Not able to live independently. Forgetful of current or recent events, become lost easily, forget names, neglectful of hygiene or eating
Severe: severely disabled and needs continuous care for all ADL
Risks of alzheimers
Advancing age Family history Female Head injury Low education level Production of apoE4 High levels of homocysteine Low levels of folic acid Oestrogen/progestin therapy Sedentary lifestyle Nicotine in cigarette smoke
Aetiology of alzheimers
Cortical atrophy causing loss of memories stored
Increase of glutamate & decrease of ACH
Tau protein introduced and forms neurotic plaques and neurofibrillary tangles
CM of alzheimers
Memory loss Confusion Disoriented Impaired judgement Personality changes Decline in ADLS Behaviours Sundowners
Dx of alzheimers
Eliminate other causes Diagnosis based on history and clinical findings MMSE Biomarkers CT PET MRI Metabolic screening Genetics Alzheimer algorithm
Tx of alzheimers
Goal of treatment to improve symptoms, no known cure
Cholinesterase inhibitors – prevent the breakdown of ACH by acetylcholinesterase (donepezil, rivastigmine).
NMDA receptor agonist – modulates the effect of glutamate at the NMDA receptor (memantine).
Antipsychotics – for neuropsychiatric symptoms (risperidone, olanzapine).
Aetiology of parkinson’s
Exact cause unknown, combination of genetics and environmental factors (exposure to toxins), head trauma, CVA. Degeneration of the basal nuclei. Pathology shows failure of neurons that secrete dopamine. Decreased dopamine results in excess of cholinergic activity
CM of parkinson’s
Gradual, insidious onset. Tremor Rigidity Bradykinesia Short shuffling gait Dysarthria Dysphagia Depression Stooped posture
Dx of parkinson’s
No specific diagnostic tests. Based on history and clinical features. Two of the triad of symptoms of tremor, rigidity and bradykinesia present. SPECT Olfactory testing.
Tx of parkinson’s
No cure. Management of symptoms. Medications: Carpidopa/Levodopa, Bromocriptine, apomorphine, amantadine, domperidone. Group support Education Exercise Nutrition DBS
Aetiology of MS
A progressive degenerative autoimmune disease characterised by disseminated demyelination of the nerve fibres of the CNS. Unknown cause. Suggested that it is related to infections (viral), immunological and genetic factors. Inflammatory process leads to destruction of myelin forming cells. Permanent disability after 20yrs or more.
Activated T cells penetrate the blood brain barrier (normal) but then inflammatory response initiates and myelin sheath of axons of motor, sensory and autonomic nerves are phagocytosed, with first-stage lesions then second-stage demyelination. Periods of exacerbation, then remission. May be exacerbated by infection, trauma, pregnancy.
CM of MS
Insidious and gradual. Varying symptoms over years.
- first signs -
paraesthesia, optic disturbances, abnormal sensations in extremities, on one side of the face, - early signs -
muscle weakness, vertigo, and other visual disturbances, such as nystagmus, muscle weakness, vertigo, fatigue, diplopia (double vision), and partial blindness.
Dx of MS
Based on history
CM and MRI to detect lesions
Spinal tap (CSF)
CT
Tx of MS
No cure, treat symptoms.
Therapy tailored to individual.
Medications: Interferon beta, mitoxantrone, corticosteroids
What is meningitis
Inflammation of the pia mater, the arachnoid and the CSF-filled subarachnoid space.
Types of meningitis
Acute purulent/BACTERIAL meningitis:
Acute lymphocytic / VIRAL meningitis:
Aetiology of bacterial meningitis
Most caused by Neisseria meningitidis (meningococcus) or Streptococcus pneumoniae. Organism gains entry through the upper respiratory tract or bloodstream into the CNS. Inflammatory response increases CSF and moderate increase in ICP.
Aetiology of viral meningitis
Most common causes are Herpes Simplex Virus, enterovirus, coxsackievirus, EBV, measles, mumps, & West Nile virus
CM of bacterial meningitis
Fever Chills Tachycardia Headache N&V Photophobia Nuchal rigidity Non-blanching petechial or purpuric rash Abdominal pains Decreased LOC and coma Seizures Death
CM of viral meningitis
Manifests similar to bacterial meningitis Mild throbbing headache Mild photophobia Mild neck pain Stiffness Fever Malaise
Dx of bacterial meningitis
H&P Blood cultures CT scan Lumbar puncture (CSF) Sputum & nasopharyngeal specimens for culture
Dx of viral meningitis
H&P, Blood H&P Blood cultures CT scan Lumbar puncture (CSF) Sputum & nasopharyngeal specimens for culture, CT scan, lumbar puncture (CSF), sputum & nasopharyngeal specimens for culture
Tx of bacterial meningitis
Analgesia
IV fluids
Antibiotics - rifampicin, ciprofloxacin, ceftriaxone, corticosteroids