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Neuro Flashcards

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1
Q

Definition: Brain death

A
  • Whole brain death involving both brainstem and higher cortical function
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2
Q

Definition: Locked in state

A
  • Disorder of motor output, where consciousness and cognition are preserved
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3
Q

Definition: Coma

A
  • No wakefulness or response to stimuli
  • Eyes-closed state of unresponsiveness
  • Dysfunction of the brainstem and higher cortical areas bihemispherically
  • Patients may remain in this state after a severe brain injury for about two weeks, and then may proceed to brain death, full recovery, or a state in between
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4
Q

Definition: Persistent Vegetative State

A
  • Recovery of brainstem activity, but not consciousness
  • Brainstem functions are preserved, but higher cortical functions are not
  • Eyes open state of unresponsiveness
  • May open eyes to external stimuli, exhibit reflexive (unintentional) movements, and regain autonomic functions including respiratory/cardiac activity and sleep/wake cycles
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5
Q

Definition: Minimally conscious state

A
  • Patients with evidence of consciousness (evidence of intention, attention, memory, awareness of self/others/environment)
  • May track objects in visual field, say a word or phrase, grasp a ball
  • Prognostic uncertainty for recovery (may remain in minimally conscious state or recovery)
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6
Q

Diagnostic assessment of patients with a disorder of consciousness

A
  • Careful and skilled neurologic exam
  • Use of the Coma Recovery Scale-Revised
  • neuro-imaging (such as fMRI and PET) may be useful
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7
Q

Pain relief in patients with disorders of consciousness

A
  • Very few studies to guide an approach to pain management in patients with impaired consciousness
  • Look for a localised response to pain
  • Frowns/shouts independent of specific stimuli may not signify pain
  • No standardised guidelines or approach . . . be attentive to the diagnosis and potential for distress

Be sure to distinguish between minimally conscious state (can perceive pain) and vegetative state (cannot perceive pain)

Assume a patient in a minimally conscious state can understand what is being said at the bedside

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8
Q

Palliative Care: Acute devastating brain injury (Examples, expected course, neuro care, and a palliative care roles)

A

Examples:
- Intraventricular hemorrhage

Expected course:
- Imminently dying, depressed LOC

Neurological care:
- Diagnosis, breaking news, prognosis, disease-specific management, formal goals of care

Palliative Care:

  • Symptom management
  • Location of dying
  • Family support
  • Bereavement care
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9
Q

Acute/relapsing brain injury with recovery (Examples, expected course, neuro care, and a palliative care roles)

A

Examples:

  • Ischemic stroke
  • Multiple sclerosis

Expected course:
- Acute functional deterioration with potential for at least partial recovery, recurrence, and future progression

Neuro care:
- Diagnosis, breaking news, prognosis, specific management, continuity of care, goals of care

Palliative care:

  • Symptom management
  • Advance care planning
  • Location of care
  • Location of death
  • Family support
  • Bereavement care
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10
Q

Neurodegenerative disorders (Examples, expected course, neuro care, and a palliative care roles)

A

Examples:

  • ALS
  • Parkinson’s
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11
Q

Neurologic palliative care: Areas of common concern

A

ABCDEF

  1. Airway
    - Secretions and aspiration
    - Symptom management, recognise limitations of feeding tube to minimize risk
  2. Breathing
    - Respiratory failure (esp. ALS) or pna
    - Provide symptom management with or without mechanical ventilation (e.g. home bipap)
  3. Comfort
    - Reduce pain and discomforts, especially those related to immobility
  4. Cognition
    - Identify limited capacity for decision making
  5. Communication
    - May be due to motor (dysarthria) or language (dysphasia)
    - Develop communication strategies for symptom assessment and expression of personal goals
  6. Decision making
    - Anticipate changes in status and document overall goals of care
    - If foregoing/withdrawing care, plan for symptom management
  7. Expectations
    - Recognise the limitations of medical interventions and consequences of care decisions on expressed goals
  8. Feeding
    - Feeding tubes may be appropriate in some circumstances
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12
Q

Responding to fears that patient with neurologic event will starve to death

A
  • Empathic listening and communication
  • Ensure clear understanding of diagnosis
  • Explore what SDMs know of loved one’s wishes and prognosis
  • Offer opinion of what death is from (e.g. stroke/aspiration pneumonia, not starvation)
  • Acknowledge uncertainty and possible outcomes of various feeding options
  • Discuss risks of nutritional support (aspiration, discomfort, etc.)
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13
Q

Options for feeding after a stroke

A
  1. PO intake
    - May ‘swallow at risk’ with potential for aspiration
    - Most appropriate when goals are for comfort, rather than prolonging of life
    - Oral intake guided by patient desire
    - Use positioning and adjusted consistency of food to minimise risk
  2. NG feeds
    - Would be initiated within 7 days for patients unable to meet nutritional requirements orally
    - Likely best approach for when goals are to prolong life
    - Does not prevent aspiration, but may prolong life
    - May be used as a time limited trial, but stopping feeding may be more emotionally difficult than never having started it
  3. PEG tubes
    - Not recommended early after stroke (increased risk of death or poor outcome)
    - Appropriate if NG feeds are maintaining weight/nutritional status and ongoing feeding is meeting patient’s goals
    - Prior to insertion, discuss circumstances in which PEG feeding might be discontinued
  4. No feeds
    - May be acceptable when goal of care is for comfort or swallowing at risk results in significant distress
    - May consider IVF in selected cases
    - Pay attention to mouth care to reduce pain from cracked lips
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14
Q

Essential components of advance care planning

A
  1. Personal values and wishes with regard to care at end of life
  2. Disclosing to patient/family their prognosis (if desired)
  3. Discussing various treatment options (risks, benefits, expected outcomes)
  4. Deciding on future care or goals of care if patient is not able to engage in discussion at some future time
  5. Documenting discussions/decisions in a way that is accessible to HCPs in various settings of care
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15
Q

Essential components of advance care planning

A
  1. Personal values and wishes with regard to care at end of life
  2. Disclosing to patient/family their prognosis (if desired)
  3. Discussing various treatment options (risks, benefits, expected outcomes)
  4. Deciding on future care or goals of care if patient is not able to engage in discussion at some future time
  5. Documenting discussions/decisions in a way that is accessible to HCPs in various settings of care
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16
Q

ALS: Diagnosis

A
  • Neurodegenerative disease with progressive loss of voluntary motor function
  • Most commonly occurs in adults age 55-75 years
  • Mixed upper and lower motor neuron deficits

Presentation:

  • UMN (hyperreflexia and spasticity – due to degeneration of lateral corticospinal tracts in spinal column) and LMN (weakness, atrophy, fasciculations – muscle denervation)
  • Early on, dysphagia and respiratory muscle weakness, later, psych/emotional/cognitive issues
  • Regional onset (bulbar - spasticity, weakness of speech and swallowing; limb - weakness of arms/legs; diaphragm - respiratory onset)
  • Progressive symptoms with UMN and LMN dysfunction, spreading to other segments of the body over time
  • Absence of neuropathic or radiculopathic pain, sensory loss, sphincter dysfunction, ptosis, or extraocular never/muscle dysfunction
  • Supranuclear gaze paresis, tremor, cerebellar ataxia, autonomic dysfunction, and extrapyramidal symptoms suggestion an ALS-plus syndrome
  • Prognosis is 2-5 years

Treatment – Disease modifying:

  • Riluzole (pill form - survival benefit, delay to trach, and may slow progression – more beneficial early on, does not treat symptoms)
  • Edaravone (IV infusion - may be used as adjunct to riluzole, improves QOL and delays progression, no clear data on survival)

Treatment – Symptomatic

  • NPPV (improves quality of life, may prolong survival though not conclusively demonstrated)
  • Chest physio may be helpful
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17
Q

Common decision points in ALS

A
  1. Nutritional support
    - Malnutrition occurs due to dysphagia/hypermetabolism and is a poor prognostic factor
    - Discuss feeding tube placement early
  2. Respiratory support
    - NIV can improve QOL
    - May not prolong life in bulbar onset ALS
    - Will not support breathing indefinitely, and even a trach with long term ventilation will not change the course of ALS
    - Discussion of NIV should include clear discussion of outcomes, that it cannot be continued indefinitely, and how withdrawal from NIV is done to prevent suffering
  3. Medication
    - Riluzole (survival benefit, may slow progression - more beneficial early on), but does not relieve symptoms)
    - Edaravone
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18
Q

Treatment for ALS

A

Treatment – Disease modifying:

  • Riluzole (pill form - survival benefit, delay to trach, and may slow progression – more beneficial early on, does not treat symptoms)
  • Edaravone (IV infusion - may be used as adjunct to riluzole, improves QOL and delays progression, no clear data on survival)

Treatment – Symptomatic

  • NPPV (improves quality of life, may prolong survival though not conclusively demonstrated)
  • Chest physio may be helpful
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19
Q

Management of joint pain in ALS (Mechanism, Management)

A

Mechanism:
- Immobility, spasticity

Treatment

  • Physical therapy (active and passive ROM)
  • NSAIDs, steroid injections, analgesics
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20
Q

Management of muscle spasms/cramps in ALS (Mechanism, Management)

A

Mechanism:
- Immobility, spasticity

Treatment:

  • Anti spasticity agents (baclofen)
  • Botox for focal spasticity
  • Muscle relaxants
  • Benzos
  • Gabapentin
  • Levetiracetam for muscle cramps
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21
Q

Management of aching/non-specific muscle discomfort in ALS (Mechanism, Management)

A

Mechanism:

  • Immobility
  • Dependent edema
  • Nocturnal hypoventilation

Treatment:

  • Massage
  • Limb elevation
  • Positioning
  • Compression stockings
  • NIV
  • TCAs (amitriptyline)
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22
Q

Management of neuropathic pain in ALS (Mechanism, Management)

A

Mechanism

  • Nerve compression syndromes
  • Spinal stenosis
  • Radiculopathy

Management:

  • Positioning
  • Splints as appropriate
  • Local anesthetic or steroid injections
  • Gabapentin/pregabalin
  • TCAs
  • Analgesics
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23
Q

Management of headache in ALS (Mechanism, Management)

A

Mechanism

  • Nocturnal hypoventilation
  • Positioning
  • Tension
  • Migraine

Management

  • NIV
  • Massage
  • Trigger identification and avoidance
  • Analgesics
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24
Q

Secretions in ALS (Mechanism, Management)

A

Mechanism

  • Impaired swallowing
  • Nasal congestion/post nasal drip
  • Respiratory failure

Management

  • Oral hygiene
  • Cleansing agents
  • NIV
  • Anticholinergics (Atropine drops, scopolamine, glyco, amitriptyline)
  • Antihistamines
  • Bronchodilators
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25
Skin irritation in ALS (Mechanism, Management)
Mechanism - Immobility (pressure points) - Drooling (perioral) Management - Positioning - Barrier ointments/creams
26
Symptoms of respiratory impairment in ALS
- Breathlessness - SOBOE or talking - Dry mouth - Supine breathlessness - Temperature intolerance - Restlessness - Muscle pain/aching - Fatigue - Daytime sleepiness - Anxiety - Morning HA - Frequent nocturnal awakening/insomnia - Poor concentration and memory - Hallucinations
27
Management of drooling in ALS
1. Anticholingeric meds - Amitriptyline - Subcut glycopyrrloate - Atropine drops - Subcut scopolamine (crosses BBB) 2. Radiation of salivary glands 3. Botox to salivary glands
28
When to consider NIV in ALS
- NIV is typically initiated for nocturnal hypoventilation, but patients will eventually need it through the daytime - Ultimately, patients will tolerate less and less time without and require it full time, and then require invasive ventilation - Long term vent with a trach may require a change in living situation - One study showed improve survival if NIV started at FVC > 65%
29
Management of breathlessness in ALS
1. NIV - As disease progresses, patients will become increasingly dependent (ie. requiring it for more hours per day) 2. Opioids for breathlessness, +/- benzos for anxiety with breathlessnesss 3. Secretion management - Chest physio (manual cough, lung volume recruitment) - Portable suction device - Mask nebulizer with mucomyst (NAC) to mobilize secretions
30
Management of insomnia/fatigue in ALS
``` Insomnia: - Consider underlying causes and treat them (Muscle cramps, pain, resp distress, depression) Meds: - Amitriptyline - Mirtaziapine - Hypnotics ``` Fatigue - Modafinal - Methylphenidate
31
Pseudobulbar affect manifestations and treatment
- Due to corticobulbar degeneration - inappropriate laughter or crying incongruent to mood Management - Educate family/caregivers/patient that patient is unable to control outbursts and do not reflect actual mood - Dextromethorphan/quinidine combination - Antidepressants (less evidence) - citalopram and amitriptyline
32
Parkinson's Disease - presentation
- Tremor (typically unilateral, resting tremor) - Rigidity (later, progressive dysphagia) - Bradykinesia (dyskinesias and dystonias may be painful) - Postural instability - Response to levodopa/carbidopa - Orthostatic hypotension and dysautonomia (typically occurs late) - Psych symptoms - panic attacks, depression, anxiety - Dementia is late finding Prognosis: 10-20 years after diagnosis
33
Multiple Systems Atrophy - Presentation
- Early dysautonomia (orthostatic hypotension, sexual impotence, bladder dysfunction) - Cerebellar dysfunction - Extreme forwward neck flexion - Prominent dysrathria - 20% respond to levodopa
34
Progressive Supranuclear palsy (presentation)
- Supranuclear vertical opthalmoplegia - Early falls, speech, and swallowing disturbances - Cognitive or behavioural changes - Rare response to levodopa, though classic parkinsonian symptoms may respond
35
Corticobasal degeneration (presentation)
- Apraxia - Cortical sensory changes - Pronounced asymmetric rigidity - Limb dystonia - Negligible response to levodopa
36
Vascular parkinsonism (presentation)
- Lower half parkinsonism with gait dysfunction predominating - Additional neurologic deficits - Evidence of vascular changes on CT - Poor response to levodopa
37
Dementia with Lewy Body (presentation)
- Early dementia - Ridgidity more prominent than bradykinesia/tremor - Spontaneous hallucinations, fluctuating cognition and falls - REM sleep behaviour disorder - Pronounced sensitivity to EPS effects of neuroleptics - Motor symptoms will respond well to levodopa, but significant psych side effects (hallucinations, confusion)
38
Treatment of motor symptoms of PD
- Levodopa/carbidopa - More frequent and lower doses can improve motor fluctuations, as can CR preps, a dopamine agonist (pramipexole/ropinorole), and amantadine - In cases of severe dystonia, botox may be helpful
39
Treatment of dysphagia in PD
- No evidence to suggest survival benefit or improved QOL with feeding tube placement - Individual decision based on discussion with patient/caregivers
40
Treatment of depression/panic/anxiety in Parkinsonism
- Conflicting data on Rx, but SSRIs are likely the safest options
41
Management of hallucinations in Parkinson's-related disorders
- Dose reduction of anti-parkinsonian meds - DC anticholinergics, followed by amantadine and dopamine agonists (pramipexole/ropinorole) if necessary - Stop levodopa as a last resort - Low doses of atypical neuroleptics (e.g. quetiapine 25mg/daily) may help
42
Management of restless leg syndrome in parkinsons
- Low dose dopamine agonists (pramipexole, ropinorole) before bedtime - Valproic acid - Benzos - Gabapentin If issue is REM sleep behaviour disorder, avoid anticholinergics and dopaminergic drugs
43
Management of cognitive dysfunction in PD
- Consider cholinesterase inhibitors (but may worsen tremor and nausea)
44
Prognosis of PD vs Parkinson's Plus:
PD - 10-20 years following dx | Parkinson's Plus - 6-10 years
45
Medications to avoid in Lewy Body Dementia
- Avoid neuroleptics (increased sensitivity, presents with impaired consciousness and severe acute parkinsonism) - Avoid anticholinergics and TCAs in the context of orthostatic hypotension - Benzos often cause paradoxical agitation If antipsychotics are required, use only atypicals (olanzapine, quetapine) in very low doses
46
Treatment of falls in PSP
- Consider amitriptyline in early stages of disease
47
Management of falls in PD and related disorders
- Consider OT for safety devices, etc.
48
Treatment of myoclonus in parkinson's plus
- Benzos (clonazepam) - Levetiracetam - Botox injections for blepharospasm
49
Treatment of dysautonomia
- Reduction of Levodopa - Compression stockings - Increased sodium intake - Improved hydration If conservative Rx fails, can trial fludrocort or midodrine
50
Treatment of REM sleep behaviour disorder
- Melatonin (3-15mg HS) | - Clonazepam HS
51
Constipation in neurodegen diseases
- PEG - Senna - 5-HT agonists (prucaloprid) - Opioid antagonists (methylnaltrexone)
52
Dyspnea in neurodegen disorders
- Opioids
53
Fatigue in neurodegen disorders
- SSRI (citalopram 20mg/day) - Modafinil 100mg daily - Methylphenidate 5mg BID
54
Muscle cramps in neurodegen disorders
- Quinidine 200mg daily
55
Pain in neurodegen disorders
- Consider source of pain (e.g. spasticity) - Opioids - Analgesic antidepressants - Tramadol
56
Pseudobulbar affect
- Dextromethorphan/quinidine 20/10mg daily (increase to BID after a week) - SSRI second line
57
Pseudohypersalivation
- Amitriptyline 25mg daily - Sage tea - Botox to salivary grands - Salivary gland radiotherapy - Scopolamine patch
58
Psychosis/agitation/irritability/dysphoria in neurodegen disorders
- Quetiapine 25-50mg/day - Clozapine - Olanzapine - Avoid typical antipsychotics in PD or PD plus
59
Treatment of rigidity/bradykinesia/akinesia in neurodegen disorders
- If PD, levodopa/carbidopa - Amantadine - Midaz
60
Spasticity in neurodegen disorders
- Baclofen (start at 5mg BID, titrate upwards) - Tizanidine (2mg HS, titrate upwards to BID) - Botox if focal - PT
61
Alzheimer's - presentation
- Most common type of dementia - Slow, progressive impairment in memory - At autopsy, accumulation of amyloid plaques, loss of neurons, neurofibrillary tangles
62
Vascular dementia - presentation
- Second most common type of dementia - Stepwise progression in cortical infarcts, slow progressive change with lacunar infarcts/white matter changes due to chronic ischemia
63
Lewy Body dementia
- Progressive cognitive decline - Vivid hallucinations - Parkinsonism - Fluctuating cognition - *Note that in PD, motor symptoms precede dementia symptoms by at least 12 months - Very sensitive to neuroleptics (may even develop neuroleptic malignant syndrome, more commonly impaired consciousness or worsened Parkinsonism)
64
Frontotemporal dementia
- Focal degeneration of frontal and/or temporal lobes - Younger age of onset (50s and 60s) - Progressive personality change, typically disinhibition or apathy - Executive function deficits - Memory/visuospatial function spared in early disease
65
Median survival of AD and markers of prognosis
4-6 years after diagnosis Poorer prognosis: - Aspiration - UTIs - Sepsis - Pressure sores - Fever - Weight loss
66
Staging of dementia
- Functional Assessment Scale (FAST scale) Stage I: - No subjective/objective difficulties Stage 2: - Complaints of misplacing objects - Subjective word finding difficulties Stage 3: - Difficulties with job performance evident to coworkers - Difficulty with organizatin Stage 4: - Impairments in IADLs Stage 5: - Needs assistance with dressing to weather/occasion Stage 6: Difficulty with BADLs Stage 7: - Speech limited to six intelligible words per day or less - Inability to ambulate independently - Inability to sit up without assistance - Inability to smile and hold head up
67
Pain in dementia
- Patients at risk of under treatment - Patients with dementia report less pain, yet still experience it (perceptual processing and sensitivity still intact) - Consider use of visual analogue scales, pain thermometors, and Faces pain scales - Use observational signs of distress Treatment options: - Tylenol is first line - Avoid NSAIDs given gastric and cardiac risk - In case opioids are prescribed, consider scheduling doses as patients may be unable to request PRN doses
68
Neuropsych symptoms
- Consider antecedents of behaviour, behaviour itself, and consequence to examine unmet needs or triggers Non-pharm management - Music therapy - Massage - Physical activity Drug therapy - Antipsychotics (avoid if possible - increased risk of death) - Avoid in Lewy Body due to severe and life threatening deterioration with antipsychotics - Consider SSRIs for depression
69
Treatment of cognitive decline in Demtnai
Cholinesterase inhibitors (donepezil) or NMDA antagonists (memantine) - Use CIs (donepezil) or memantine for mod/severe AD - modest improvement in cognition, function, and behaviour - CIs may improve outcomes in Vascular dementia and Lewy Body disease Taper off (and do not start) in advanced disease due to high risk of adverse effects (GI symptoms, falls, bradycardia, etc.)
70
Feeding tubes in dementia
- No survival benefit, do not prevent aspiration pneumonia, do not improve comfort or reduce risk of pressure ulcers - Avoid, and promote hand feeding and proper oral care
71
Advanced care planning in dementia
- Thoroughly explore patient values and goals with family members prior to a crisis situation - Discuss specific aspects of care (CPR, ICU, artificial nutrition, IV fluid, etc.) - Hospitalization should be avoided in advanced dementia if possible, as may result in significant decline - Consider hospice for advanced dementia
72
Intracranial hypertension - pathophys
ICP - Balance between liquid component (CSF and blood - dependent on systemic BP) and solid (brain) - Adult cranium is a vault with a fixed size - Any disruption to balance can result in increased cranial pressure - If growth is slow, may be compensated initially by enhanced CSF absorption, increased drainage, etc. - If process is sudden or when compensatory measures become insufficient, ICP becames an issue Causes: - Tumours (with consequent edema) - Abscesses - Hematomas
73
Intracranial HTN - Presentation
Presentation - Altered LOC (most common, initial presentation with psychomotor retardation and slowed verbal/motor responses, progressing to stupor and coma) - HA (diffuse, more intense supine, worse in AM. Worsened by head movements, cough, Valsalva) - N/V - Papilloedema (low sensitivity) - Focal neuro signs (most frequently diplopia) - Seizures
74
Signs and symptoms of ICP waves
- Waves of very high ICP, lasting seconds to minutes Presentation - Altered LOC, agitation, delirium - HA - Neck pain - Seizures (focal or generalised) - Decerebration (hypertonus, extension, internal rotation of four limbs) - CN II, IV, VI nerve paralysis and eye deviation - Nystagmus, tinnitus - Myoclonus of face and limb muscles - Dysarthria - Dysphagia - Cardioresp disturbance - Hyperthermia - N/V/D
75
Types of brain edema
Vasogenic edema - Increase in fluid of the extracellular space due to increased capillary permeability - E.g. with HTN, esp. with brain tumours Cytotoxic edema - Due to intracellular volume from ischemic/hypoxic cellular damage Interstitial edema - Increase of the extracellular volume due to CSF obstruction (no reabsorption) Osmotic edema - Increase in water content of the brain parenchyma due to plasma hypo-osmolarity (e.g. hyponatremia and SIADH)
76
Treatment of raised ICP
1. Positioning - Head at least 30 degrees over heart to facilitate drainage 2. Infusion of hypertonic solutions - Mannitol IV - caution in renal disease, CHF, intracerebral hemorrhage, time limited to < 3 days - Hypertonic saline 3% 5-10mL/kg, watch for rebound effect after a few days 3. Steroids - Reduces inflammation and outflow of blood components at the site of damage - Onset of action in 48-72 hrs - Dex is ideal, better concentration in CSF
77
Seizures: Types
1. Focal onset - Focal onset aware seizures - Focal onset impaired awareness - May become secondarily generalised 2. Generalised onset 3. Unknown onset Seizures may be motor or non-motor (absence, if with awareness, sensation, etc.)
78
Treatment of seizures in Palliative Care
1. Levetiracetam - Broad spectrum and status epilepticus - PO, subcut off label 2. Phenytoin - Broad spectrum and status epilepticus - Firstline for most seizures - IV (watch BP) or PO 3. Phenobarb - PO and subcut (diluted with saline) - Cytochrome P450 - Slow plasma clearance (4-5 days) prolonged by liver disease - Can cause drowsiness, ataxia, and SJS 4. Lacosamide - Adjunct for focal seizures with and without secondary generalization - May be useful in depression
79
Status epilepticus
- Seizures lasting longer than 5 minutes (little chance of spontaneous resolution) Management: - ABCs, IV access - Lorazepam or Midaz - Then Keppra or Valproic acid (avoid in liver failure) - Then Phenytoin IV in NS THEN: - Consider Phenobarb, 20mg/kg (caution with respiratory depression), effect delayed until 20-30 mins after admin
80
Clinical course of brain metastases
- Median survival 2 months with no treatment - With good response to radiotherapy, patients usually die of systemic disease rather than direct effects of brain mets - Survival after whole brain rads usually 4-6 months
81
Presentation of brain mets
- May be sudden and stroke like or more subtle and only picked up on neuro exam - Headache is common - aching, moderate to severe, worse in AM and overnight
82
Treatment of brain mets
Rads (whole brain or stereotactic) - Survival after whole brain rads typically 4-6 months - Response especially good with breast and lung ca Surgery if only a single met with limited or no systemic disease, especially if the tumour is radioresistant Steroids - Recommended for all symptomatic patients - Ideally start 48 hrs prior to rads (Dex 8-16mg/day with taper after 7 days by 2mg q 5 days) to minimum effective dose - Consider increase in dose if symptoms recur or evidence of high ICP
83
Leptomeningeal carcinomatosis pathophys
- Dissemination of cancerous cells through the subarachnoid space - May occur due to peripheral circulation, perineural invasion, invasion from epidural lesions, or seeding from brain tumours - May be multifocal or diffuse - Most common with lung, breast, lymphoma, leukemia, or melanoma - Prognosis 3-6 months following dx
84
Most common symptoms of leptomeningeal carcinomatosis
- Highly variable clinical syndromes - Change in mental status, headache, radicular pain - Cranial nerve involvement - Polyradiculopathy - Seizures - Multiple symptoms from different levels of the neuraxis
85
Diagnosis of leptomeningeal carcinomatosis
- CSF sample (malignant cells, high opening pressure, high protein content, increased WBC, low glucose - Contrast enhanced MRI (sensitivity 90%)
86
Treatment of leptomeningeal carcinomatosis
- Steroids - Rads may be helpful - Systemic chemo or intrathecal chemo (dubious evidence)
87
Lesions at the base of skull
- Local invasion from head and neck cancer - Mets from breast, prostate cancer Symptoms - Cranial nerve deficits - Headache (either at sight, at the vertex, or to the entire affected side of head) - Trigeminal nerve involvement (dull pain with paroxysmal lancinating or throbbing pain) with 'Numb chin syndrome' with involvement of the mental nerve - Glossopharyngeal nerve involvement may lead to throat and neck pain with difficulty swallowing
88
Myasthenia Gravis
- Associated with thymoma (15%) - Antibodies against the acetylcholine receptors Presentation: - Fatiguable weakness without sensory or coordination abnormalities - Worse with use, better on awakening or following rest or cold temp - Diplopia, Ptosis - Dysphagia to solids (LR 13) - Slurred speech after talking (LR 4.5) Diagnosis: - Tensilon test: Give edrophonium (acetylcholinesterase inhibitor) and check for reversal of grip strength weakness within 30 seconds, lasting 5 mins. Requires cardiac monitoring for bradycardia/asystole, rx with atropine if needed Treatment - Acetylcholinesterases (meostigmine) - Steroids - Thymectomy - PLEX if severe/urgent with respiratory compromise
89
Lambert Eaton Myasthenic Syndromes
- Associated with Small cell lung ca (3%) - Occurs due to antibodies against presynaptic membrane, results in impaired acetylcholine release (in myasthenia, antibodies are to the RECEPTOR) Presentation - Muscle weakness, fatigue, and pain - Legs commonly affected (in contrast to myasthenia) - Mainly proximal muscles affected, improves with repeated use ("warm up period") - Symptoms worsened with high temperatures - Cranial nerves affected less commonly than in myasthenia (ptosis, diplopia) - Depressed/absent reflexes - Autonomic changes (constipation, dry mouth, blurred vision) Diagnosis: - EMG - Antibody testing - on exam, strength improves with repeated handgrip Treatment: - Immunosuppression - Plasmapheresis
Palliative
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