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MED627 > TLOC/DOC/TBI rehab > Flashcards

TLOC/DOC/TBI rehab Flashcards

1
Q

Define TLOC and what is it also known as?

A
  • TLOC is spontaneous LOC with complete recovery
  • due to acute global impairment of CBF
  • rapid onset, brief duration and spontaneous recovery
  • also known as blackout or syncope
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2
Q

outline the epidemiology of TLOC

A
  • accounts for 3% of ER visits and 1% all hospital admissions
  • lifetime cumulative incidence unto 35% in general population
  • peak incidence: young adults 10-30yrs, often fam history of 1t degree relation (inherited)
  • Common with increasing age: sharp rise in elderly after 70yrs
  • slightly higher in female than males
  • heterogeneity in the causes of blackout presented in primary care or emergency departments - cardiovascular is a major cause
  • survival worst for patients with the cardiovascular cause of syncope when compared b/w participants w and w/o syncope
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3
Q

what are the main clinical challenges in TLOC?

A
  1. Main witness unconscious - person who had a blackout cannot tell the history, can describe the before and after
  2. Eyewitness account unreliable but essential - therefore, dependent on collateral witness
  3. Unpredictable, hence difficult to record
  4. Occasionally life threatening - cardiac sudden collapse on floor w football players
  5. Driving restrictions, health & safety - HGV drivers
  6. Initial diagnosis often inaccurate, delayed - waiting for neurologist is 6 months while patients should be seen within 4 weeks of blackout and A&E often refer to first fit clinic
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4
Q

what are the risks of TLOC?

A
  1. can be the first symptom a fatal cardiac arrhythmia (problem w rate or rhythm of heart beat) - more than 100,000 deaths every year in the UK -> sudden death often attributed to cardiac arrhythmias
  2. syncope may result in injury to patients or others as result of accidents (during the event)
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5
Q

what are the characteristics of sudden death due to cardiac arrhythmias

A
  1. most common killer in the US (350,000 deaths / annum)
  2. event rates in Europe similar
  3. significant geographic variations
  4. inherited cardiomyopathies / arrhythmias in people under the age of 30 years
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6
Q

what are the differential diagnosis of TLOC?

A

A DROP IN BP

  1. neurally mediated (reflex) syncope
    - population based study shows it is the most common cause
  2. cardiac syncope
    - due too structural disease or arrhythmia - second most common cause (specially in ER and elderly)
  3. orthostatic hypotension
    - increases w increase in age due to reduced baroreflex response, decreased cardiac compliance, attenuated vestibulosympathetic reflex
    - more common in institutionalised (50–70%) than community dwelling (6%)
    - cause for increased mortality due to associated comorbid conditions (AF,VF, prolonged QT interval)
  4. neurological
  5. metabolic disorders - rarer
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7
Q

what are the different types of neurally mediated (reflex) syncope?

A
  1. vasovagal - when you faint cause your body overreacts to certain triggers like the sight of blood or extreme emotional distress
  2. situational
    - cough - consecutive coughing can lead to drop in BP
    - micturition - common in men
  3. carotid sinus hypersensitivity - exaggerated response to carotid sinus baroreceptor stimulation -> diminished cerebral perfusion
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8
Q

what are the different types of neurological syncope?

A
  1. epilepsy
  2. sleep disorders
  3. raised intracranial pressure - rare but if patient is unwell
  4. psychogenic non epileptic attacks
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9
Q

what are the different types of neurogenic orthostatic hypotension (nOH)?

A
  • also called postural hypotension, a drop in BP when you stand up or lie down
    1. drugs - hypertensive
    2. neurodegenerative disorders (ANS dysfunction)
  • PD - nOH in PD is due to an inadequate release of NE (NA - increases HR + BP) resulting in failure of the ANS to maintain s-SBP
  • multiple system atrophy (MSA)/ postural hypotension - rare
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10
Q

what are the crucial steps in history taking of LOC

A
  • patients wouldn’t describe LOC rather perhaps blackout
    1. before the attack
    2. during the attack
    3. after the attack
    4. frequency
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11
Q

what are the signs to look out for before the attack while doing the history of TLOC?

A
  1. prodrome is common although LOC w/o any warning signs may also occur
    - typical symptoms: dizziness, lightheadedness or faintness, weakness, fatigue, visual and auditory disturbances
    - typical aura: sweaty, warm?
  2. any provoking features (trigger) e.g. stress upset? mood
  3. circumstances under which the attack occurred - at work place or home?
  4. can the attacks be prevented? (triggers0
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12
Q

what are the signs to look out for during the attack while doing the history of TLOC?

A
  1. whether they actual had an actual LOC
  2. duration of attack - secs/mins if described as hour - perhaps wrong
  3. verbal/tactile responsiveness - response to voice or nudging
  4. movement/ limb jerking
  5. pulse
  6. tongue biting and urine incontinence - not reliable unless it is really severe as much to be seen at dental – that’s more likely to be epilepsy
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13
Q

what are the signs to look out for after the attack while doing the history of TLOC?

A
  1. Recovery - rapid / prolonged
  2. Confused or sleepy
  3. duration
  4. How much does the patient remember (muscle pain)
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14
Q

what is epidemiology of vasovagal syncope?

A
  1. No comprehensive theory for vasovagal syncope
  2. 0.5% of the population faint per annum (women > men)
  3. 1:200 referrals to A&E;
  4. 75,000 attendances per annum in UK
  5. Syncope alone is responsible for
    - 3 to 5 % of emergency room visits
    - 1 to 3 % of hospital admissions
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15
Q

what are three main factors that result vasovagal syncope? (3Ps)

A
  1. posture - sudden change in posture e.g. orthostatic hypotension
  2. provocation - hot weather, vasovagal
  3. prodromal - any wild illness, even cough and cough contribute to drop in BP, cardiac and neurological syncope
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16
Q

what are the characteristics of convulsive syncope?

A
  1. Convulsive movements are common
  2. Diagnosis depends on history
  3. Lack of post-ictal confusion, hearing people around you before you can respond and recurrence of blackout on regaining upright posture helpful in diagnosis
  4. Common sense
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17
Q

what causes micturition syncope?

A
  • relaxation not straining unless male patient has an enlarged prostate or stricture
  • role of pelvic venous plexus
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18
Q

what is long QT syndrome?

A

ECG recording show a long QT, if not diagnosed early enough it results in death - fatal arrhythmia

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19
Q
  1. what happens in cardiac syncope?
  2. its causes?
  3. features of onset?
A
  1. temporary but sudden reduction in blood supply and hence oxygen to the brain as a result of cardiovascular conditions
  2. triggering syncope is caused by vasodilation, hypotension and arrhythmia (bradycardia, tachycardia or valvular disease)
  3. onset of syncope is relatively rapid and recovery from LOC is spontaneous, complete and usually prompt
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20
Q

what is a common misdiagnosis of epilepsy?

A
  • Non-epileptic attack disorder (NEAD),Psychogenic non epileptic seizures
  • more common than epilepsy
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21
Q

What helps or doesn’t help in the history of diagnosing NEAD?

A

Helpful
1. Scant description from patient - patient cannot give you the history , normally would answer don’t know, look at family for answers
2. Frequent or long seizures
3. Different types of seizures - epilepsy by definition episodes need to be stereotypes – need to be exactly same every time
4. Crying during recovery - Become upset after the seizure episode NEAD – crying
Not helpful
1. injury
2. Tongue biting
3. Incontinence
4. Seizures ‘in sleep’

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22
Q

what are the clinical features of NEAD?

A
  1. Common – you are more likely to witness NEAD than an epileptic seizure
  2. Gradual onset, undulating motor activity with pauses
  3. Sinusoidal and asynchronous arm and leg movements
  4. Prolonged atonia, rhythmic pelvic movements, side to side head movements
  5. Post ictal crying, high anxiety in carers
  6. Prolonged attack with prolonged / unexpectedly sudden recovery
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23
Q

what is the risk of misdiagnosing of NEAD?

A
  1. Inappropriate treatment - risk of adverse effects of antiepileptic drugs, including teratogenicity
  2. Ineffective treatment
    When there is an effective treatment
  3. Reinforcement of abnormal illness behaviour
    - Evolution of functional symptoms
    - Incapacity
    - Financial and social dependency
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24
Q

what the features of EEG?

A
  1. Not normally used to distinguish epilepsy from other TLOC
  2. Non specific abnormalities common
  3. Very useful if it captures an event
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25
Q

what is the significance of neuroimaging in TLOC?

A
  1. Not normally used to distinguish epilepsy from other TLOC
  2. Non-specific and co-incidental abnormalities common
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26
Q

what is the difference b/w awareness, wakefulness and sleep?

A

awareness - ability to have or having the experience of any kind
wakefulness - state in which eyes are open and there is a degree of motor arousal
sleep - a state in which eyes are closed and motor inactivity

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27
Q

what is coma and what are its features?

A
  • deep sleep-like state from which patient cannot be aroused
    1. Unrousable
    2. Unresponsive
    3. >6 hours
    4. Cannot be wakened
    5. Lacks normal sleep-wake cycle
    6. No voluntary actions
28
Q

what is vegetative state and what are its features?

A
  • an awake but non-responsive state in a patient who has emerged from coma
  • open eyelids (giving the appearance of wakefulness)
  • respiratory + autonomic functions retained
  • yawning, coughing, swallowing, limb and head movements preserved
  • patient may follow visually presented objects
  • if any meaningful response to external and internal environment - awake coma
    1. can be diagnosed after 4 weeks (continuing)
    2. permanent if > 1 year following TBI or >6 months in other mechanisms - persistent vegetative state
    3. Controversial language
29
Q

what is minimally conscious state and what are its features?

A
  • patient has basic (rudimentary) vocal or motor behaviour (often spontaneous)
    1. Severely altered consciousness
    2. Minimal evidence of self and environmental awareness
    3. Inconsistent but reproducible responses to surroundings
    4. Follow simple commands - “yes/no” suggesting little areas of cortex preserved
    6. Crying, smiling, laughing in response to emotional stimuli - preserved emotional responses
    7. Reaching for objects with intent
    8. Eye movement pursuit
    9. Can be diagnosed after 4 weeks of PDOC -“Continuing”
    11. Permanent if > 5 years in most cases and > 3-4 years in diffuse injury, no improvement seen
30
Q

what are the preconditions for diagnosis of VS or MCS?

A
  1. cause of condition known: e.g. brain injury, degenerative conditions, metabolic/infective disorders
  2. reversible causes excluded: influence of drugs, metabolic causes, treatable structures eg collection of blood/hydrocephalus
  3. careful assessment: by trained assessor experienced in management of PDOC, under appropriate conditions (positioning, environment), using validated tests in a series of observations over an appropriate period of time
31
Q

what are the anatomical elements involved in DOC?

A
  • Ascending reticular activating system (ARAS) contains contains cholinergic and monoaminergic neurons
  • Intralaminar nuclei of the thalamus maintains arousal
  • cholinergic neurones in the medial pontine tegmentum to the thalamus
  • monoaminergic neurones projecting from the upper brainstem to thalamus, basal forebrain and cortex
32
Q

Medication s that interfere w Ach (anti-cholinergic) can result in cognitive impairment and arousal
True or False

A

True

33
Q

what are the physiological elements involved in DOC?

A
  1. Stimulation of the posterior hypothalamus causes arousal
  2. Lesions in the cuneus and precuneus association cortex involved in MCS
  3. Lesions in anterior cingulate can result in abulia (lack of motivation)
34
Q

which are the essential anatomical affected conditions required for LoC?

A
  1. Brainstem – significant to disrupt ARAS
  2. Thalamus – disrupt the cortical projections, mostly commonly seen
  3. Bilateral hemispheres – higher neocortical impairment but if one side then stroke (classical hemisphere lesion causing focal deficits)
35
Q

what are the common causes of persistent DOC (PDOC)?

A
  1. trauma - direct impact or deceleration injury, coup/contra - coup injury (have a good prosperous of recovery)
  2. vascular - ICH, SAH, CVA
  3. hypoxic or hypo-perfusion - cardiac arrest, shock
  4. infection or inflammation - encephalitis, vasculitis (LOC not profound cause by definition it has to be bilateral cortical hemispherical lesion and infection usually don’t spread that much)
  5. Toxic or metabolic - drug or alcohol poisoning, severe hypoglycaemia - reversible however, much worse in severe hypoglycaemic - unaware they are experiencing
36
Q

what is mimic-locked in syndrome and what are its features?

A
  • pseudocoma
    1. consciousness intact - aware of self and environment
    2. no voluntary movement nor able to communicate verbally due to complete paralysis of all voluntary muscles except vertical eye movements and blinking
    3. high brain stem pathology - central pontine myelinolysis
    4. often iatrogenic - during rapid overcorrection of hyponatraemia - therefore, important medical-legal case
37
Q

what is the difference between apallic syndrome or mimic-locked in syndrome?

A

apallic syndrome - preserved brain stem + destruction of brain cortex
mimic locked-in syndrome - destruction of brain stem + preserved brain cortex

38
Q

what are assements involved in PDOC?

A
  1. history - collateral
  2. observation - temp, BP, RR, HR, SpO2 (peripheral capillary oxygen saturation)
  3. general examination - chest, abdomen, extremities
  4. GCS
  5. meningism
  6. trauma
  7. fundoscopy/pupils
  8. tone
  9. reflexes
  10. brainstem
39
Q

how is the smell assessed in general examination of PDOC?

A
  • general examination involves smelling of breath
  • Certain smells are associated with certain toxins or poison
    1. bitter almond - cyanide
    2. burnt rope - opium
    3. fruity - paraldehyde (agriculture industry)/ ketones
    4. garlic - phosphorus
    5. pepper - tear gas
    6. vinegar - hydrofluoric acid
    7. hay - phosgene (agriculture industry)
40
Q

how is the skin assessed in general examination of PDOC?

A
  • the overuse of drugs are associated with various skin condition
    1. skin bullae (blister) - barbiturates
    2. tracks - opium
    3. sweating - cholinergic
    4. flushing - amphetamine
    5. dry - anti-cholinergic
    6. hot - tricyclics
41
Q

when was the GCS score devised?
what does it consist of?
how is the GCS score assessed in PDOC?

A
  • devised in 1974
  • consists of eye (4), vocal (5) and motor score (6)
  • highest 15 and lowest 3
  • motor is the most important factor
  • if person is drowsy then eye score is not reliable
  • if stroke then vocal may get attenuated
  • however, motor score is helpful to guide the neurosurgeons and neuro-anethetics
  • therefore, overall GCS score is not adequate rather need to provide the score for each of the segments
42
Q

how is the meningism assessed in PDOC?

A
  1. nuchal rigidity - neck stiffness
  2. brudzinski sign - raising the head while the legs are bent
  3. kerning’s sign - lifting the leg causes shooting pain in the neck
    - high prevalence of cervical spine disease in elders may result in false positive for nuchal rigidity
    - sensitivity and specificity of all three tests uncertain
43
Q

how is the pupil assessed with fundoscopy in PDOC?

A

essential to detect

  1. papilloedema - raised ICP
  2. horners syndrome
  3. third nerve palsy - down and out
  4. uncle herniation
44
Q

why does uncus herniation need to be treated immediately?

A

refer

45
Q

how are the tone and reflexes assessed in PDOC?

A
  • increased tone and brisk reflexes = UMN
  • decreased reflexes - could be due to anticholinergic overdose
  • may be misleading early on, therefore, repetitive assessment is vital
46
Q

how is the brain stem assessed in PDOC?

A

to asses the

  • breathing - different BP associated w lesion in different areas
  • gaze
  • eye movements
  • oculocephalic reflex
47
Q

what are the localisation in coma?

A
  1. bihemipsheric
  2. supratentorial mass lesion e.g. tumour - unilateral signs, third nerve palsy
  3. brain stem - asymmetric , eye movement disorder, large pupil (downward shift), small pupil (upward shift), normal CT= basilar artery occlusion
  4. metabolic -
48
Q

what are the tests carried out for DOC?

A
  1. lab tests - acidosis, anion gap, osmolar gap - anti-freeze
  2. concentration of Na+, Ca2+, Co2 and glucose
  3. drug screen
  4. blood cultures
  5. imaging, EEG and CSF - look for infection, structural changes
49
Q

what is rehabilitation?

A
  • The process of helping a person reach the fullest physical/psychological/social/vocational/ educational potential consistent with anatomic or physiological impairment, environmental limitations and desires and life plans.
  • The process of active change by which a patient acquires knowledge and skills necessary for optimal physical, psychological and social function
  • longterm holistic approach
  • People want different things from different demographic societies and everyone’s views about life and personal achievements are not the same
50
Q

what is the aim of rehabilitation?

A
  • Aim to reduce activity restrictions (disability)
  • Aim to teach new skills and strategies eg walking with an aid, transfers, catheter
  • To prevent complications
  • Alter the environment- home adaptations, work
  • Goal-setting (SMART)
    Specific; Measurable; Achievable; Relevant; Time limit
51
Q

what is an acquired brain injury?

A
  • an injury to the brain that is not hereditary, congenital, degenerative or induced by birth trauma
  • an injury that has occurred after birth
52
Q

give five examples of acquired brain injury

A
  1. Traumatic brain injury (TBI)
  2. Haemorrhagic brain injury (HBI)
  3. Vascular brain injury (VBI)
  4. Anoxic (& metabolic) brain injury (ABI)
  5. Infective brain injury (IBI)
53
Q

define TBI

A

an alteration in brain function, or other evidence of brain pathology, caused by an external force

54
Q

what is aetiology of TBI?

A
  1. Leading Cause - RTC (road transport corporation) approx. 25-30%
  2. Falls 30-35% (elderly)
  3. Assaults 9-10%
  4. Sports and recreational - 10-20%
  5. In USA, firearms 10%
  6. Few studies specifically focus on mild TBI
55
Q

define TBI

A

TBI is defined as an alteration in brain function, or other evidence of brain pathology, caused by an external force, Common Data Elements 2013

56
Q

what is contusion?

where is it?

A
  • bruising of the brain
  • close to bony prominences - inferior frontal and temporal poles
  • evident on the underside of the brain
  • the base of skull consists of ridges, nerves and various BVs which run to the BS in neck
  • if a face is applied, the brain will shear across all the se ridges
57
Q

what is diffuse axonal injury?

A
  1. Severe rotation or deceleration force
    Often RTC
    Often loss of consciousness or prolonged low awareness
    Little haemorrhage
58
Q

what are the different types of intracranial bleed?

A
  1. extradural haematoma - most dangerous but good recovery if drained
  2. subdural haematoma
  3. sub arachnoid bleed
  4. intracerebral/ intraventricular bleed
  5. skull fracture - infection, CSF leaks
59
Q

what is the difference b/w primary and secondary injury?

A

primary - injury at the moment of impact or immediately afterwards e.g. coup
secondary - further injury caused by subsequent events including poor care e.g. contra coup

60
Q

how to differentiate seizure and syncope?

A
  1. movements
    - seizures: tonic-clonic hallmark for generalised
    - syncope: myoclonic and other movements occur in 90% episodes (arrhythmic and <30s)
  2. aura
    - seizures: (partial or complex partial w secondary generalisation) unpleasant smell, fear, anxiety, abdominal discomfort or. other visceral sensation
    - syncope: dizziness, lightheadedness or faintness, weakness, fatigue, visual and auditory disturbances, sweaty
  3. autonomic manifestations: most challenging
    - seizure: cardiovascular, GI, pulmonary, pupillary (similar. premonitory of syncope)
    - cardiovascular manifestation of autonomic epilepsy include significant tachycardias and bradycardia similar to cause of LOC
    - therefore, presence of accompanying non-autonomic auras may help differentiate
  4. duration
    seizure: LOC associated w seizure (tonic-clonic) lasts >5mins and associated w prolonged post octal confusion and lethargy
  5. muscle ache: occur after both but last longer following a seizure
  6. provoking factors: syncope can be provoked by emotion or pain but less likely for seizures
  7. urine incontinence: in both but focal incontinence may occur only in seizure
    features of epilepsy
  8. description of an aura - epileptic patients struggle to describe their attack, however, if the patient sits w hands crossed and expect the other person to describe it is NEA
  9. Head-turning or posturing of body
  10. Abnormal behaviour of which patients do not remember: some very agitated or paranoid after epilepsy
  11. Severe tongue bite
    syncope: reorientation occurs immediately after a syncope event
61
Q

what are various conditions that simulate coma/coma mimic?

A
  1. vegetative state
  2. MCS
    - cardiac arrest + cerebral hypoperfusion and head injuries are most common of these two
  3. akinetic mutism: partially or fully awake state, able to think and form impressions but remain virtually immobile and mute, normal sleep-wake cycle but no motor activity
    - results from: damage in medial thalamic nuclei or frontal lobes or extreme hydrocephalus
  4. abulia: milder form of akinetic mutism w mental and physical slowness and diminished ability of activity initiation
  5. catatonia: hypomobile and mute syndrome that occurs due to psychosis, usually SCZ or major depression
  6. mimic locked-in syndrome: destruction of brain stem + preserved brain cortex
  7. apallic syndrome - preserved brain stem + destruction of brain cortex -> cortical parts of the brain detached from the brainstem
  8. dementia - thought to be an altered state of cognition but fulfils the criteria of DOC as eventually they stop interacting and become unaware
  9. hyper insomnia - respiratory issues, OSA (obstructive sleep apnea)
    when awake and no external evidence of mental activity
62
Q

describe the anatomy and physiology of coma?

A
  • all instances of diminished alertness -> abnormalities of cerebral hemispheres or reduced activity of RAS
  • proper functioning of this system, its ascending projections to cortex and cortex itself required to maintain alertness and coherence of thought
  • principal causes of coma
    1. lesions that damage RAS in upper mid brain or its projections
    2. destruction of large portions of both cerebral hemispheres
    3. suppression of reticulocerebral function by drugs, toxins or metabolic derangements e.g. hypoglycaemia, anoxia, uraemia and hepatic failure
  • RAS closely situated to the midbrain structures that control pupillary function and eye movements
  • this pupillary enlargement w loss of light reaction + loss of vertical and adduction eye movements suggests the lesion is in upper BS
  • conversely, preserved pupillary light reactivity and eye movements absolved the upper BS and indicated widespread structural lesions or metabolic suppression of cerebral hemisphere as a cause for coma
63
Q

what is the significance of herniation in coma?

A
  • herniations refers displacement of brain issue into a region that it normally does not occupy
    1. uncal transtentorial: shift of uncus (anterior midline temporal gyrus) into tectorial opening (anterior and adjacent to the opening)
  • uncus compresses of CN 3 (occulomotor) -> enlargement of ipsilateral pupil
  • affects the ventricular system -> hydrocephalus
    2. central
    3. transfalcial
    4. foraminal
64
Q

what is involved in history taking of coma patients?

A
  1. history
    - collateral evaluation essential
    - most cases causation evident e.g. trauma, cardiac arrest, reported drug ingestion
    - remainder, certain points useful
    a. circumstances and rapidity of neurological symptoms development
    b. prior symptoms (confusion, weakness, headache, fever, seizures, dizziness, double vision or vomiting)
    c. use of medications, illicit drugs or alcohol
    d. chronic disease (liver, kidney, lung, heart)
65
Q

what does the general examination in coma patient involve?

A

general physical examination

  1. TEMPERATURE
    - fever: systemic infection, bacterial meningitis, encephalitis, malignant hyperthermia (due to anaesthetics or anti-cholinergic intoxication)
    - hypothermia due to alcohol, sedatives intoxication, hypoglycaemia, peripheral circulatory failure or extreme hypothyroidism
    - hypothermia itself. causes coma when <31C
  2. BREATHING RATE
    - tachypnea (abnormal rapid breathing): may indicate systemic acidosis or pneumonia
  3. BP
    - hypertension: hypertensive encephalopathy, secondary to rapid rise in ICP (the Cushing response) after haemorrhage or BI
    - hypotension: alcohol or barbiturate intoxication, ICH, myocardial infarction, sepsis

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