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Year 2 > Neuro: Part 5 > Flashcards

Neuro: Part 5 Flashcards

1
Q

Motor effects in primary generalised seizures

A

BILATERAL SYMMETRICAL and synchronous motor manifestations

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2
Q

What are partial (focal) seizures

A

These are localised to a part of one hemisphere

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3
Q

What causes partial seizures

A

Structural diseases

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4
Q

How can a partial seizure progress

A

Can become secondary generalised tonic-clonic seizures

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5
Q

What are tonic-clonic generalised seizures

A

Causes bilateral tonic and clonic muscle contractions

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6
Q

What is the Tonic phase of the seizure

A
  1. Consciousness lost and skeletal muscles will suddenlyy tense - patient falls
  2. Upward deviation of the eyes (open)
  3. Mouth open
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7
Q

How long does he tonic phase of a seizure last

A

10-20 seconds

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8
Q

What is the clonic phase of a seizure

A

Muscle relaxation of tense muscle from tonic and re-contraction - convulsions

Bilateral,, rythmic muscle jerking

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9
Q

Clinical presentation of primary generalised tonic-clonic seizure

A
  1. Often no AURA stage (sudden progression to post-itically)
  2. Loss of consciousness
  3. Eyes open
  4. Tongue bitten
  5. Incontinence/faeces
  6. Drowsiness, coma or confusion post-itically
  7. Characteristic groan as they fall to ground
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10
Q

What is petit mal

A

Generalised seizure in which there is brief loss and return of consciousness and NO POSTICTAL state

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11
Q

When is petit mal seen

A

Children

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12
Q

Clinical presentation of petit mal

A
  1. Child ceases activity, stares and pales (stops talking and then carries on)
  2. Unawaree of attack
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13
Q

Diagnostic of petit mal

A

EEG - shows 3-Hz spike

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14
Q

How does petit mal progress as a condition as child becomes adult

A

Develop generalised tonic-clonic seizures in adult life

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15
Q

What are myoclonal seizures

A

Seizures in myoclonic families - those who have brief, involuntary twitching of a group of muscles

Isolated jerk of limb, face or trunk

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16
Q

Clinical presentation of myoclonic seizure

A

Patient thrown suddenly to the ground or have a disobedient limb

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17
Q

What are tonic seizures

A

Sustained increase tone with a groan as they fall to the ground

Intense stiffening of body

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18
Q

What are tonic seizures not followed by jerking

A

Because there is no clonic phase

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19
Q

What is an atonic seizure

A

Sudden loss in muscle tone and cessation of movement - fall to th aground

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20
Q

What are simple partial seizures

A
  1. Focal serisures that do not effect consciousness or memory
  2. Asymptomatic and no post-octal symptoms
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21
Q

What are complex partial seizures

A
  1. Affect awareness and memory before, during or immediately after seizure
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22
Q

Where do complex partial seizures occur

A

Usually in the temporal lobe (speech, memory and emotion)

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23
Q

Post-Ictal signs of complex partial seizures

A

Confusion

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24
Q

In which complex partial seizure is recovery more rapid

A

Temporal and frontal lobe

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25
Q

What happens to a partial seizure in 2/3 of patients

A

Becomes secondary generalised seizure - conclusions seen

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26
Q

Clinical presentation of complex partial seizures in the temporal lobe

A

REMEMBER: effects memory, emotions and speech understanding
1. AUTO: Deja vu, auditory hallucinations, funny smell and fear
Anxiety or out of body experience, automatisms (chewing fiddling etc)

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27
Q

Clinical presentation of complex partial seizures in the frontal lobe

A

REMEMBER: Motor and though processing

  1. Posturing or peddling movements of leg
  2. Jacksonian march (seizure goes up and down motor homunculus)
  3. Post-ictal todd’s palsy - paralysis of limbs involved in seizure for a few hours
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28
Q

Clinical presentation of parietal lobe focal seizure

A
  1. SENSORY DISTURBANCES - tingling/numbness
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29
Q

Clinical presentation of occipital lobe focal seizure

A

Visual phenomenas (lines, flashes or spots)

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30
Q

How do we distinguish epilepsy over syncope

A
  1. Tongue biting
  2. head turning
  3. Muscle pain
  4. Loss of consciousness
  5. Cyanosis
  6. Post-ical symptoms
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31
Q

How do we distinguish syncope from epilepsy

A
  1. CAUSES: Prolongues standing, sweat prior to unconsciousness and nausea
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32
Q

What causes non-epileptic seizures

A

Situational dependnat

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33
Q

Signs of epileptic vs non-epileptic seizures

A
  1. Non: Longer, close mouth and eyes during tonic-clonic movements and pelvic thrusting - NO INCONTIENCNE OR TONGUE BITING

Sleep is not a factor

PRE-ICTAL ANXIETY symptoms in non

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34
Q

Differential diagnosis of epilepsy

A
  1. Postural syncope
  2. Cardiac arrhythmia
  3. TIA
  4. MIGRAINE
  5. Hyperventilation
  6. Hypoglycaemia
  7. Panic attacks
  8. Non-epileptic seizure
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35
Q

Rule of thumb when diagnosing epilepsy

A
  1. Has to be at least 2 or more unprovoked seizures occurring more than 24 hours apart - HISTORY taking
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36
Q

What diagnostics are sued for seizures

A
  1. EEG
  2. MRI
  3. CT Head
  4. FBC
  5. Genetic testing
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37
Q

Why is an EEG done for seizures

A

NON-diagnostic but supports diagnosis

Seizure type and what epilepsy syndrome seen

3Hz spike

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38
Q

Why is an EEG not diagnostics

A

Becomes normal between attacks

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39
Q

Role of MRI in seizures

A

Imaging of hippocampus

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40
Q

Role of hippocampus

A

Short-term to long-term memory

Spatial memory for navigation

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41
Q

Role of CT in seizures

A
  1. SPACE OCCUPYING LESIOSN (tumour caused seizure??)

2. Structural abnormalities

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42
Q

Role of FBA in seizures

A
  1. Hypoglycaemia
  2. RENAL and liver function tests
  3. Rules out comorbities
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43
Q

When is genetic testing useful for seizures

A

Myoclonic epilepsy (remember, family dependant)

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44
Q

How is seizures treated when not knowing the actual type of seizure present

A
  1. ABCDE
  2. Glucose monitor
  3. DIAZEPAM (rectally or IV)
  4. IV PHENYTOIN (prophylaxis anti-epileptic drug)

——2nd line——-
Anaesthetist involvement and ventilation

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45
Q

When should drugs for seizure not be given

A

When it is one-off

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46
Q

Treatment of generalised tonic-clonic seizure

A

ORAL SODIUM VOLPROATE (teratogenic)

ORAL LAMOTRIGINE

ORAL CARBAMAZEPINE

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47
Q

Side-Effect of generalised tonic-clonic seizure

A

Weight gain
Hair loss
Liver failure

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48
Q

Side effects of oral LAMOTRIGINE

A

Maculopapular rash
Blurred vision
Vomiting

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49
Q

Side effects of ORAL CARBAMAZEPINE

A 
Diplopia
Rashes
Leucopenia
Impaired balance
Drowsiness
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50
Q

What are maculopapular rash

A

Flat red area on skin with small bumbs

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51
Q

Treatment of petit mal

A
  1. ORAL SODIUM VALPROATE
  2. ORAL LAMOTRIGINE
  3. ORAL ETHOSUXIMIDE
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52
Q

Side effect of ORAL ETHOSUXIMIDE

A

Rashes

Night terrors

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53
Q

How are partial/focal seizures treated

A
  1. CARBAMEZEPINE
  2. SODIUM VALPROATE
  3. LAMOTRIGINE
54
Q

Surgical procedures for seizures

A
  1. Surgical resection of tumour

2. VAGAL NEVRE STIMULATION - reduces seizure frequency

55
Q

What fatal condition can repeated seizures result in

A

Status epilepticus (MEDICAL EMERGENCY)

56
Q

What is status epileptics

A

Continuous seizures without recovery of consciousness

57
Q

Risks if we get grand-map one after another

A

risk of death from CV failure

58
Q

What causes status epileptics

A
  1. Stopping preventative treatment
  2. ALovhol abuse
  3. Poor compliance to therapy
59
Q

Lifestyle changes to patients with epilepsy

A

MUST INFORM DVLA - can’t drive until a year without seizures

Do not swim alone and avoid dangerous sports (rock-climbing)

60
Q

What is SUDEP

A

Sudden unexpected death epilepsy: Nocturnal apnoea or asytole during night

61
Q

Define dementia

A
  1. A syndrome caused by a number of brain disorders which causes memory loss, difficulties with thinking, problem-solving or language as well as difficult ire with activities of daily living
62
Q

What is the most common form of dementia

A

Alzheimer’s

63
Q

What structures are damaged in alzheimer’s

A

Causes degeneration of cerebral cortex with cortical atrophy

64
Q

Pathophysiology of alzheimer’s

A

1, Accumulation of beta-amyloid peptides = progressive neuronal damage, neurofibrillary tangles increase sin number of amyloid plaques causes loss of ACh

65
Q

What is vascular dementia

A

Brian damage due to cerebrovascular disease (stroke, multi-infarcts or changes in small vessel structure)

66
Q

How do we diagnose vascular dementia

A

Raised BO
Past strokes
Focal CNS signs

67
Q

What is lewy-body dementia

A

Deposition of abnormal proteins within neurone in brainstem and neocortex

68
Q

Clinical presentation of lewy body dementia

A 
Fluctuating cognitive impairment
Visual hallucinations 
Impairment to frontal lobe 
Parkinsons 
Loss of inhibition 
Depression 
Variation in attention and alertness
69
Q

What disease is lewy body dementia associated with

A

PARKINSON’s

70
Q

What is fronts-temporal (pick’s) dementia

A
  1. Degeneration and atrophy of frontal and temporal lobes
71
Q

Clinical signs of fronts-temporal dementia

A
  1. BEHAVIOURAL and personality change
    Early preservation of episodic memory and spatial orientation
  2. Emotional unconcern
  3. Lower inhibition

THIS IS A FORM OF MIXED DEMENTIA as it effect many places

72
Q

Rarer forms of dementia

A
  1. Liver failure caused
  2. HIV caused
  3. Prion disease (CREUTZFELDT-JAKOB)
  4. Vitamin B12/folate deficiency
  5. HUNTINGON’s
73
Q

Risk factors for dementia

A
  1. AGE
  2. FAM HISTORY
  3. DOWN SYNDROME
  4. Alcohol
  5. High BP
  6. Diabetes
  7. Atherosclerosis
  8. Depression
  9. High oestrogen levels
74
Q

Clinical presentation of alzheimer’s

A
  1. Short-term emory loss early symptoms
  2. Personality deterioration
  3. Intellect gone
  4. Decline in speech
  5. Visuospatial skills
  6. Apraxia
  7. Agnosia
75
Q

Define agnosia

A

Failure to recognise objects

76
Q

Define apraxia

A

Impaired ability to cary out skilled motor tasks

77
Q

Differential diagnosis of dementia

A
  1. Substance abuse (Alcohol)
  2. Hypothyroidism
  3. Space-occupying lesions intracranial
  4. Huntington’s
78
Q

How is dementia diagnosed

A
  1. HISTORY - cognitive function assessment
  2. MMSE (mini mental state examination
  3. Exclusion of rare causes of dementia (substance abuse, vit B12)
  4. FBC Liver biochemistry, B12, thyroid function
  5. Neuropsychology
  6. Brain CT in younger patients
  7. MRI (atrophy)
  8. Brian functions
79
Q

How is brain function assessed in dementia patients

A

PET and SPECT scanning - blood supply

Functional MRI - brain networks

80
Q

How doe the Mini Mental State Examination work

A

Score of 25 or above out of 30 normal

18-24 = mild impairment

17 = serious impairment

81
Q

How is dementia treated

A
  1. SUPPORT
  2. LIFESTYLE CHANGES (preventative)
  3. MEDICATIONS
82
Q

What support can we give dementia patients

A
  1. Talking to far and friends
  2. Board games - stimulation
  3. Specialist memory service
  4. CARERS
83
Q

Preventative therapy for dementia

A
  1. Helath behaviour
  2. Smoking cessation, diet and low alcohol
  3. 6 leisure activities a week = lower risk
  4. Education, mental activities and occupation decreases risk
  5. Changes in amyloid-beta are seen 25 years before onset (early monitoring)
84
Q

What medications can be given for alzheimer patients

A
  1. ORAL DONEPEZIL or RIVASTIGMINE (ACh inhibitors - increases ACh)
  2. RAMUPRUL - vascular dementia (prevents worsening)
85
Q

Define Parkinson’s Disease

A
  1. Degenerative movement disorder caused by reduction in DOPAMINE IN SUBSTANTIA NIGRA
86
Q

What characterises Parkinsons

A
  1. RIGIDITY
  2. BRADYKINEASIA (slow to execute movement)
  3. Resting tremor
87
Q

When is peak onset of parkinson’s

88
Q

What gender does Parkinson’s effect

89
Q

Risk factors of Parkinson’s

A
  1. Male
  2. Increasing age
  3. Family History
  4. Being a non-smoker
  5. Drug induced
  6. Environmental factors
90
Q

What environmental factors can induce parkinson’s

A

1, Pesticides
MPTP - opiates

Mitochondrial dysfunction + Oxidative stress!!!!

91
Q

How do alterations in genes cause parkinson’s

A
  1. Mutation in parkin and alpha-synuclein gene
92
Q

What forms the basal ganglia

A
  1. STRIATUM
  2. GLOBUS PALLIDUS
  3. SUBSTANTIA NIGRA
  4. SUBTHALAMIC NUCLEUS
93
Q

Pathophysiology of Parkinson’s

A
  1. MITOCHONDRIAL DYSFUNCTION AND OXIDATIVE STRESS causes progressive degeneration of dopaminergic neurone from pars compacts of Substantia nigra that project to striatum
  2. Reduced striatum dopamine levels
  3. Thalamus is more inhibited = parkinson’s
94
Q

How does Parkinson’s worsen

A

LEWY-BODIES become more widespread from lower brainstem to midbrain and then into cortex

95
Q

How can we tell the severity of parkinson’s

A

extent of dopaminergic cell loss correlated with degree of akinesia (muscle rigidity, stiffness and lack of responsiveness)

96
Q

What are lewy-bodies made of

A

ALPHA-SYNUCLEIN and UBIQUITIN

97
Q

Clinical presentation of Parkinson’s

A

INITIAL:
Impaired dexterity and unilateral foot drop

ASSYMETRICAL

Anosmia (reduced sense of smell)
Depression
Aches and pain 
REM sleep disorders
Urinary urgency 
Hypotension and constipation

LATER:
TREMOR
RIGIDITY
BRADYKINESIA

98
Q

When are tremors in parkinson’s worse

99
Q

Where are tremors seen

A

ASYMMETRICALLY in hands

100
Q

What makes tremors better

A

Voluntary movement

101
Q

What makes treours worse

102
Q

How to distinguish parkinson’s from cerebellar trmeours

A

4-6 cycles a sec

Repetitive hand movement worsens in rhythm the longer attempted

103
Q

Why do we get rigidity in Parkinson’s

A

We get lesions in extrapyramidal tract (increased muscle tones in limbs and trunk)

104
Q

Clinical presentation of rigidity in Parkinson’s joint

A
  1. Limbs resist passive extension throughout movement (does not go away like in clasp-knife phenomenon)
  2. Pain and problems in bed
105
Q

Characteristics of Bradykinesia in Parkinson’s

A
  1. Slow to initiate movement of repetitive actions:
    REDUCED LINK RATE
    MONOTONOUS HYPOPHONIC SPEECH
    MICROGRAPHIA (writing smaller)
  2. Changes in gait
  3. Expressionless face (hypo mimesis)
106
Q

Characteristics in Gait in Bardykinesia

A
  1. REDUCED ASYMMETRICAL ARM SWING
  2. NARROW GAIT
  3. STOOPED POSTURE and SMALL STEPS
  4. FESTINANCE
107
Q

What is Festinance

A
  1. Shuffling steps

2. Dragging foot with flexed trunk

108
Q

Facial characteristics in Parkinson’s

A
  1. Drooling of saliva
  2. Swallowing difficulty (late event)
  3. Aspiration pneumonia
  4. Depression
  5. Constipation
  6. Urinary frequency increased
109
Q

Differential diagnosis of Parkinson’s

A
  1. Benign essential tremor
  2. LEWY BODY DEMENTIA
  3. Drug-induced
  4. WILSON’s disease
  5. Trauma
  6. Dopamine antagonists
110
Q

How is benign essential tremor treated

A
  1. PROPRANOLOL (contraindicated in diabetes)

2. PRIMIDONE (anti-seizure) or GABAPENTIN (anti-epileptic)

111
Q

How is Parkinson’s diagnosed

A
  1. HISTORY
  2. Response to LEVODOPA
  3. Dementia, incontiennce, symmetry and early falls
112
Q

How is Parkinson’s treated

A
  1. Compensate for loss of dopamine
  • ——PRIMARY——–
    1. Balance
    2. Speech
    3. Gait

Non respond to medication so PHYSIOTHERAPY + Physical activity

  • ——-SECONDARY——
    1. ORAL LEVODOPA with decarboxylase inhibitor (CO-CARELDOPA)
113
Q

Why is LEVODOPA given and not dopamine

A

L-DOPA is a precursor which can cross BBB

114
Q

Why is decarboxylase inhibitor given alongside LEVODOPA

A

Prevents peripheral conversion of L-DOPA (maximises dose that can cross BBB and reduces peripheral side-effects)

115
Q

Side-effects of LEVODOPA

A
  1. NAUSEA
  2. VOMITING
  3. ARRYTHMIAS
  4. PSYCHOSIS
  5. VISUAL HALLUCINATION
116
Q

Motor complications of LEVODOPA

A
  1. Reduced efficacy over time even if dose is increased
  2. ON-dyskinesias (hyperkinetic, choreiform movement - rapid, repetitive and jerky involuntary movements)
  3. OFf-dyskinesias (fixed, painful dystonic posturing (twisting and repetitive movements or abnormal fixed postures - sustained muscle contraction)
  4. FREEZING
117
Q

How long doe sit take for LEVODOPA to stop working

A

5-10 years

118
Q

What can be given instead of LEVODOPA so we can use it as a later treatment

A
  1. MAO-B and COMT inhibitors - dopamine antagonists
119
Q

Does LEVODOPA alter disease progression

A

NO - symptom relief

120
Q

Name some DOPAMINE ANTAGONIST

A
  1. ORAL ROPINIROLE

2. ORAL PRAMIPREXOLE

121
Q

Side-Effects of dopamine antagonist

A
  1. Drowsiness
  2. Nausea
  3. Hallucination
  4. Compulsive behaviour
122
Q

What dopamine antagonist should we avoid

A

Bromocriptine and cabergoline - cardiac valvulopathy

123
Q

Name an MAO-B inhibitor

A

ORAL SELEGILINE or ORAL RASAGILINE

124
Q

How do MAO-B inhibitors work

A

Inhibit MAO-B which breakdown dopamine = reduction of dopamine breakdown so dopamine remains for longer

125
Q

Side-Effect of MAO-B inhibitor

A

Postural hypotension and AF

126
Q

Name a COMT inhibitor

A
  1. ORAL ENTACAPONE or TOLCAPONE
127
Q

Role of COT inhibitr

A

Breaks down dopamine

128
Q

Side-effect of COMT inhibitor

A

TOLCAPONe causes liver damage

129
Q

Ho do we treat neuropsychiatric complications

A

ORAL CITALOPRAM = SSRIs

2. ORAL QUETIAPINE (anti-psychotics)

130
Q

Surgical treatments of Parkinson’s

A
  1. DEEP BRAIN STIMULATION to help those who are partially-dopamine responsive
  2. SURGICAL ABLATION o overreactive basal ganglia circuits (sub thalamic nuclei)

Year 2 (155 decks)

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