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
Tx of viral meningitis
Usually self-limiting and symptomatic treatment only
HSV type 2 requires antiviral drug treatment: acyclovir
What is encephalitis
Acute inflammation of the parenchyma of the brain. Serious, sometimes fatal disease.
Aetiology of encephalitis
Epidemic which are transmitted by ticks or mosquitoes
Non-epidemic which occurs as a complication of measles, chicken-pox or mumps
CM of encephalitis
Non-specific Fever Headache N&V Confusion Lethargy Disorientation Seizures Focal paralysis Delirium Cushing’s triad (hypertension, bradycardia, irregular breathing) Coma
Dx of encephalitis
H&P CT EEG MRI PET IgM antibodies to virus in serum or CSF
Tx of encephalitis
Patients usually require intensive care
Measures to control intracranial pressure and ventilation
Encephalitis due to HSV or varicella zoster virus treated with antiviral, acyclovir
Outline focal brain injury
Force of impact causes contusions. Results from compression of skull at point of impact and rebound effect. Impact against object or within skull.
Outline diffuse brain injury
Result from shaking effect caused by high levels of acceleration or deceleration. Produces strains and distortions within the brain. Can cause irreparable cognitive impairment
Outline hypoxic brain injury
Deprivation of oxygen with maintained blood flow
Outline excitotoxic brain injury
During prolonged ischemia excess glutamate is outside cell causing ion channels to remain open and over exciting brain cells. Higher energy and oxygen consumption drives uncontrolled opening of other channels. Excessive influx of Na into cells draws water in to cells. Na/Ca pump fails due to ATP deficiency, ↑Ca in cells causes auto digestion from activated enzymes. Anaerobic metabolism with glycogen instead of glucose. Death of cerebral cells in the micro neurones responsible for higher order brain function.
Outline intracranial pressure
When CPP slows and ICP increases brain tissue experiences severe hypoxia, if ICP is not evenly distributed throughout the cranial vault compartments the brain tissue moves to a compartment of lesser pressure (herniation).
Outline cerebral oedema
Increase in brain tissue volume due to abnormal fluid accumulation. Occurs after brain insult: trauma, infection, haemorrhage, tumour, ischaemia, infarct or hypoxia. CM vary: little early compensation, as ICP increases: headache, nausea and vomiting, decreased LOC, coma, pupillary changes.
Outline ischaemic brain injury
Reduced or interrupted blood flow
What is ischaemia
Situation of reduced or interrupted blood flow
Types of ischaemia
Focal Ischaemia
Global Ischaemia
What is focal ischaemia
Only a region of the brain is under-perfused
Collateral circulation provides blood flow to the borders of the focal ischaemic region
Maintains a low level of metabolic activity, preserving membrane integrity.
Interruption of glucose delivery results in depletion of ATP & increased lactic acid production
What is global ischaemia
Cardiac arrest is global and causes loss of glutamate and Na K pump
Blood flow to entire brain is compromised and is inadequate to meet the metabolic needs of the entire brain
Unconsciousness occurs within seconds when severe
If cerebral circulation restored immediately, consciousness is regained quickly.
CM of ischaemia
Acidosis (no removal of wastes)
Three components which occupy the cranial vault
Blood (10%)
Brain tissue (80%)
CSF (10%)
Normal ICP
5-15 mmHg
CM of raised ICP
Headache Nausea Vomiting Increased blood pressure Decreased mental abilities Confusionabout time, then location and people as the pressure worsens Double vision Unresponsive pupils Shallow breathing Seizures Loss of consciousness Coma
Dx of raised ICP
Assess BP and pupils
Lumbar puncture
CT
MRI
Tx of raised ICP
Frusemide
Acetazolamide
Mannitol
What is the Monro-Kellie Hypothesis
Relationship between Blood, Brain & CSF.
When small increase in one occur, the other two must reduce sufficiently to maintain stable ICP.
What is cerebral oedema
Increase in the fluid content of the brain.
Types of cerebral oedema
Vasogenic
Cytotoxic
Ischemic
Interstitial
What is vasogenic cerebral oedema
Caused by increased permeability of the capillary endothelium (BBB) of the brain after injury
What is cytotoxic cerebral oedema
Toxic factors directly affect the cellular elements of the brain parenchyma, causing failure of the active transport systems (cells loose potassium, gain sodium and water = swell). Common causes are hypoxic and ischaemic injury
What is ischemic cerebral oedema
Follows cerebral infarction (stroke). Components of both Vasogenic & Cytotxic oedema. Initially confined to the intracellular compartment, then brain cells necrose and release lysosomes = autodigestion. BBB permeability increases = oedema
What is interstitial cerebral oedema
Most often with non-communicating hydrocephalus. Oedema caused by CSF shifting into extracellular spaces. Fluid volume increases, compresses white matter, causes rapid disappearance of myelin lipids.
CM of cerebral oedema
Headache Neck painor stiffness Nauseaorvomiting Dizziness Irregular breathing Vision lossor changes Memory loss Inability to walk Difficulty speaking Stupor Seizures Loss of consciousness
Dx of cerebral oedema
Head and neck exam Neurologic exam CT MRI Blood tests
Tx of cerebral oedema
Treat the cause
Localised swelling: dexamethasone.
Osmotic diuretics useful for acute vasogenic and cytotoxic oedema
What is hydrocephalus
Various conditions characterised by excess fluid in the cranial vault or sub-arachnoid space.
Types of hydrocephalus
Communicating: Impaired absorption of CSF within sub-arachnoid space. More often in adults.
Non-Communicating: Obstruction of CSF flow between ventricles. More often in children.
CM of hydrocephalus
- Acute Hydrocephalus - Rapidly increasing ICP
Coma.
- Normal P hydrocephalus - Memory and cognitive decline Unsteady, broad-based gait Falls Apathy Inattentiveness Indifference Urinary incontinence
Dx of hydrocephalus
H&P
CT
MRI
Tx of hydrocephalus
Surgical - surgery of cysts, tumours, haematomas, bypass; Ventriculo-peritoneal (VP) Shunt, Ventriculo-atrial (VA) Shunt.
Diuretics for normal pressure hydrocephalus.
What is epilepsy
Disorder in which nerve cell activity in the brain is disturbed causing seizures. Recurrent without underlying correctable cause
What is a seizure
Sudden, transient alteration of brain function caused by an abrupt explosive, disorderly discharge of cerebral neurons
Types of seizures
Partial/Focal Seizures Myoclonic Tonic-Clonic Tonic Atonic
What is a partial/focal seizure
Only portion of the brain. Most common. Subtle, confusional conscious state
What is a myoclonic seizure
Brief muscle jerks usually involving one or a group of muscles. No LOC, may fall or drop item
What is a tonic clonic seizure
LOC, body stiffens (tonic) rapidly followed by jerking limbs (clonic). Lasts 2-3mins. Accompanied by confusion, lethargy after convulsions cease.
What is a tonic seizure
Increase in muscle tone and stiffening of body. Injury if fall
What is an atonic seizure
Loss of muscle tone, fall. No LOC, rapid recovery
Aetiology of seizures
Cerebral lesions, biochemical disorders, cerebral trauma, fever, drug or alcohol abuse, infection, postnatal trauma, congenital malformations
Dx of seizures
H&P Lab/blood tests Urine CT MRI CSF EEG
Tx of seizures
Correcting the cause
Counselling
Anti-epileptic medications: phenytoin, carbamazepine, valproic acid or valproate, benzodiazepines, oxcarbazepine, gabapentin
What is a stroke
Damage to the brain from interruption of its blood supply.
Types of strokes
Ischaemic
Hemorrhagic
What is an ischaemic stroke
Thrombotic and embolic stroke. Arterial occlusions caused by thrombi formed in arteries supplying the brain or in intracranial vessels. Include TIAs and Lacunar Infarcts. 80% of strokes
What is a hemorrhagic stroke
Intracerebral or subarachnoid haemorrhage. Ruptured blood vessel in the brain
CM of ischaemic stroke
Hemiparesis Hemianopia (blindness in 1 eye) Weakness Unilateral numbness Language disturbance (aphasia) Slurred speech (dysarthria) Sudden unexplained imbalance or ataxia
CM of hemorrhagic stroke
Headache N&V Unilateral weakness Numbness Tingling Speech and visual disturbances Motor deficits LOC due to raised ICP
Dx of ischaemic stroke
H&P CT scan MRI Angiography Lumbar puncture
Dx of hemorrhagic stroke
H&P CT scan MRI Angiography Lumbar puncture
Tx of ischaemic stroke
Supportive
Maintain cerebral perfusion
Thrombolysis
Anticoagulants: warfarin, heparin, tPA thrombolytic drugs
Tx of hemorrhagic stroke
Supportive
Control ICP
Prevent ischemia and hypoxia.
Diuretics: frusemide, mannitol
Anti-hypertensives.
Risks of stroke
Increasing age Sex Race Family history Hypertension Smoking Poorly controlled diabetes (atherosclerosis) Carotid stenosis Sickle cell disease Hyperlipidaemia Atrial fibrillation
What is brain trauma
Traumatic insult to the brain possibly producing physical, intellectual, emotional, social and vocational changes
Types of brain trauma
Open trauma: Causes primarily focal injuries
Closed trauma: Causes haematoma and focal (local) or diffuse (general) brain injuries
Types of diffuse brain injury
mild concussion: immediate but temporary CM. Confusions (1-7mins), amnesia, headache. No LOC
classical concussion: LOC up to 6hrs, reflexes fail. Breathing ceases, low HR and BP then stabilise. Amnesia, confusional state (hrs – days), head pain, nausea, fatigue, attention and memory deficits, mood changes.
diffuse axonal injuries: Prolonged traumatic coma (>6hrs)
Mild: Post-traumatic coma 6-24hrs, residual deficits
Moderate: Widespread physiological impairment, prolonged coma (>24hrs) incomplete recovery.
Severe: Brainstem contusion
