Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What are partial (focal) seizures

A

These are localised to a part of one hemisphere

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What causes partial seizures

A

Structural diseases

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

How can a partial seizure progress

A

Can become secondary generalised tonic-clonic seizures

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What are tonic-clonic generalised seizures

A

Causes bilateral tonic and clonic muscle contractions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

How long does he tonic phase of a seizure last

A

10-20 seconds

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is petit mal

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

When is petit mal seen

A

Children

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Diagnostic of petit mal

A

EEG - shows 3-Hz spike

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

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

A

Develop generalised tonic-clonic seizures in adult life

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Clinical presentation of myoclonic seizure

A

Patient thrown suddenly to the ground or have a disobedient limb

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What are tonic seizures

A

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

Intense stiffening of body

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What are tonic seizures not followed by jerking

A

Because there is no clonic phase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What is an atonic seizure

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What are complex partial seizures

A
  1. Affect awareness and memory before, during or immediately after seizure
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Where do complex partial seizures occur

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Post-Ictal signs of complex partial seizures

A

Confusion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

In which complex partial seizure is recovery more rapid

A

Temporal and frontal lobe

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
What happens to a partial seizure in 2/3 of patients
Becomes secondary generalised seizure - conclusions seen
26
Clinical presentation of complex partial seizures in the temporal lobe
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)
27
Clinical presentation of complex partial seizures in the frontal lobe
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
28
Clinical presentation of parietal lobe focal seizure
1. SENSORY DISTURBANCES - tingling/numbness
29
Clinical presentation of occipital lobe focal seizure
Visual phenomenas (lines, flashes or spots)
30
How do we distinguish epilepsy over syncope
1. Tongue biting 2. head turning 3. Muscle pain 4. Loss of consciousness 5. Cyanosis 6. Post-ical symptoms
31
How do we distinguish syncope from epilepsy
1. CAUSES: Prolongues standing, sweat prior to unconsciousness and nausea
32
What causes non-epileptic seizures
Situational dependnat
33
Signs of epileptic vs non-epileptic seizures
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
34
Differential diagnosis of epilepsy
1. Postural syncope 2. Cardiac arrhythmia 3. TIA 4. MIGRAINE 5. Hyperventilation 6. Hypoglycaemia 7. Panic attacks 8. Non-epileptic seizure
35
Rule of thumb when diagnosing epilepsy
1. Has to be at least 2 or more unprovoked seizures occurring more than 24 hours apart - HISTORY taking
36
What diagnostics are sued for seizures
1. EEG 2. MRI 3. CT Head 4. FBC 5. Genetic testing
37
Why is an EEG done for seizures
NON-diagnostic but supports diagnosis Seizure type and what epilepsy syndrome seen 3Hz spike
38
Why is an EEG not diagnostics
Becomes normal between attacks
39
Role of MRI in seizures
Imaging of hippocampus
40
Role of hippocampus
Short-term to long-term memory Spatial memory for navigation
41
Role of CT in seizures
1. SPACE OCCUPYING LESIOSN (tumour caused seizure??) | 2. Structural abnormalities
42
Role of FBA in seizures
1. Hypoglycaemia 2. RENAL and liver function tests 3. Rules out comorbities
43
When is genetic testing useful for seizures
Myoclonic epilepsy (remember, family dependant)
44
How is seizures treated when not knowing the actual type of seizure present
1. ABCDE 2. Glucose monitor 3. DIAZEPAM (rectally or IV) 4. IV PHENYTOIN (prophylaxis anti-epileptic drug) ------2nd line------- Anaesthetist involvement and ventilation
45
When should drugs for seizure not be given
When it is one-off
46
Treatment of generalised tonic-clonic seizure
ORAL SODIUM VOLPROATE (teratogenic) ORAL LAMOTRIGINE ORAL CARBAMAZEPINE
47
Side-Effect of generalised tonic-clonic seizure
Weight gain Hair loss Liver failure
48
Side effects of oral LAMOTRIGINE
Maculopapular rash Blurred vision Vomiting
49
Side effects of ORAL CARBAMAZEPINE
``` Diplopia Rashes Leucopenia Impaired balance Drowsiness ```
50
What are maculopapular rash
Flat red area on skin with small bumbs
51
Treatment of petit mal
1. ORAL SODIUM VALPROATE 2. ORAL LAMOTRIGINE 3. ORAL ETHOSUXIMIDE
52
Side effect of ORAL ETHOSUXIMIDE
Rashes | Night terrors
53
How are partial/focal seizures treated
1. CARBAMEZEPINE 2. SODIUM VALPROATE 3. LAMOTRIGINE
54
Surgical procedures for seizures
1. Surgical resection of tumour | 2. VAGAL NEVRE STIMULATION - reduces seizure frequency
55
What fatal condition can repeated seizures result in
Status epilepticus (MEDICAL EMERGENCY)
56
What is status epileptics
Continuous seizures without recovery of consciousness
57
Risks if we get grand-map one after another
risk of death from CV failure
58
What causes status epileptics
1. Stopping preventative treatment 2. ALovhol abuse 3. Poor compliance to therapy
59
Lifestyle changes to patients with epilepsy
MUST INFORM DVLA - can't drive until a year without seizures Do not swim alone and avoid dangerous sports (rock-climbing)
60
What is SUDEP
Sudden unexpected death epilepsy: Nocturnal apnoea or asytole during night
61
Define dementia
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
What is the most common form of dementia
Alzheimer's
63
What structures are damaged in alzheimer's
Causes degeneration of cerebral cortex with cortical atrophy
64
Pathophysiology of alzheimer's
1, Accumulation of beta-amyloid peptides = progressive neuronal damage, neurofibrillary tangles increase sin number of amyloid plaques causes loss of ACh
65
What is vascular dementia
Brian damage due to cerebrovascular disease (stroke, multi-infarcts or changes in small vessel structure)
66
How do we diagnose vascular dementia
Raised BO Past strokes Focal CNS signs
67
What is lewy-body dementia
Deposition of abnormal proteins within neurone in brainstem and neocortex
68
Clinical presentation of lewy body dementia
``` Fluctuating cognitive impairment Visual hallucinations Impairment to frontal lobe Parkinsons Loss of inhibition Depression Variation in attention and alertness ```
69
What disease is lewy body dementia associated with
PARKINSON's
70
What is fronts-temporal (pick's) dementia
1. Degeneration and atrophy of frontal and temporal lobes
71
Clinical signs of fronts-temporal dementia
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
Rarer forms of dementia
1. Liver failure caused 2. HIV caused 3. Prion disease (CREUTZFELDT-JAKOB) 4. Vitamin B12/folate deficiency 5. HUNTINGON's
73
Risk factors for dementia
1. AGE 2. FAM HISTORY 3. DOWN SYNDROME 4. Alcohol 5. High BP 6. Diabetes 7. Atherosclerosis 8. Depression 9. High oestrogen levels
74
Clinical presentation of alzheimer's
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
Define agnosia
Failure to recognise objects
76
Define apraxia
Impaired ability to cary out skilled motor tasks
77
Differential diagnosis of dementia
1. Substance abuse (Alcohol) 2. Hypothyroidism 3. Space-occupying lesions intracranial 4. Huntington's
78
How is dementia diagnosed
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
How is brain function assessed in dementia patients
PET and SPECT scanning - blood supply Functional MRI - brain networks
80
How doe the Mini Mental State Examination work
Score of 25 or above out of 30 normal 18-24 = mild impairment 17 = serious impairment
81
How is dementia treated
1. SUPPORT 2. LIFESTYLE CHANGES (preventative) 3. MEDICATIONS
82
What support can we give dementia patients
1. Talking to far and friends 2. Board games - stimulation 3. Specialist memory service 4. CARERS
83
Preventative therapy for dementia
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
What medications can be given for alzheimer patients
1. ORAL DONEPEZIL or RIVASTIGMINE (ACh inhibitors - increases ACh) 2. RAMUPRUL - vascular dementia (prevents worsening)
85
Define Parkinson's Disease
1. Degenerative movement disorder caused by reduction in DOPAMINE IN SUBSTANTIA NIGRA
86
What characterises Parkinsons
1. RIGIDITY 2. BRADYKINEASIA (slow to execute movement) 3. Resting tremor
87
When is peak onset of parkinson's
55-65
88
What gender does Parkinson's effect
MALES
89
Risk factors of Parkinson's
1. Male 2. Increasing age 3. Family History 4. Being a non-smoker 5. Drug induced 6. Environmental factors
90
What environmental factors can induce parkinson's
1, Pesticides MPTP - opiates Mitochondrial dysfunction + Oxidative stress!!!!
91
How do alterations in genes cause parkinson's
1. Mutation in parkin and alpha-synuclein gene
92
What forms the basal ganglia
1. STRIATUM 2. GLOBUS PALLIDUS 3. SUBSTANTIA NIGRA 4. SUBTHALAMIC NUCLEUS
93
Pathophysiology of Parkinson's
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
How does Parkinson's worsen
LEWY-BODIES become more widespread from lower brainstem to midbrain and then into cortex
95
How can we tell the severity of parkinson's
extent of dopaminergic cell loss correlated with degree of akinesia (muscle rigidity, stiffness and lack of responsiveness)
96
What are lewy-bodies made of
ALPHA-SYNUCLEIN and UBIQUITIN
97
Clinical presentation of Parkinson's
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
When are tremors in parkinson's worse
REST
99
Where are tremors seen
ASYMMETRICALLY in hands
100
What makes tremors better
Voluntary movement
101
What makes treours worse
Anxiety
102
How to distinguish parkinson's from cerebellar trmeours
4-6 cycles a sec Repetitive hand movement worsens in rhythm the longer attempted
103
Why do we get rigidity in Parkinson's
We get lesions in extrapyramidal tract (increased muscle tones in limbs and trunk)
104
Clinical presentation of rigidity in Parkinson's joint
1. Limbs resist passive extension throughout movement (does not go away like in clasp-knife phenomenon) 2. Pain and problems in bed
105
Characteristics of Bradykinesia in Parkinson's
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
Characteristics in Gait in Bardykinesia
1. REDUCED ASYMMETRICAL ARM SWING 2. NARROW GAIT 3. STOOPED POSTURE and SMALL STEPS 4. FESTINANCE
107
What is Festinance
1. Shuffling steps | 2. Dragging foot with flexed trunk
108
Facial characteristics in Parkinson's
1. Drooling of saliva 2. Swallowing difficulty (late event) 3. Aspiration pneumonia 4. Depression 5. Constipation 6. Urinary frequency increased
109
Differential diagnosis of Parkinson's
1. Benign essential tremor 2. LEWY BODY DEMENTIA 2. Drug-induced 3. WILSON's disease 4. Trauma 5. Dopamine antagonists
110
How is benign essential tremor treated
1. PROPRANOLOL (contraindicated in diabetes) | 2. PRIMIDONE (anti-seizure) or GABAPENTIN (anti-epileptic)
111
How is Parkinson's diagnosed
1. HISTORY 2. Response to LEVODOPA 3. Dementia, incontiennce, symmetry and early falls
112
How is Parkinson's treated
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
Why is LEVODOPA given and not dopamine
L-DOPA is a precursor which can cross BBB
114
Why is decarboxylase inhibitor given alongside LEVODOPA
Prevents peripheral conversion of L-DOPA (maximises dose that can cross BBB and reduces peripheral side-effects)
115
Side-effects of LEVODOPA
1. NAUSEA 2. VOMITING 3. ARRYTHMIAS 4. PSYCHOSIS 5. VISUAL HALLUCINATION
116
Motor complications of LEVODOPA
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
How long doe sit take for LEVODOPA to stop working
5-10 years
118
What can be given instead of LEVODOPA so we can use it as a later treatment
1. MAO-B and COMT inhibitors - dopamine antagonists
119
Does LEVODOPA alter disease progression
NO - symptom relief
120
Name some DOPAMINE ANTAGONIST
1. ORAL ROPINIROLE | 2. ORAL PRAMIPREXOLE
121
Side-Effects of dopamine antagonist
1. Drowsiness 2. Nausea 3. Hallucination 4. Compulsive behaviour
122
What dopamine antagonist should we avoid
Bromocriptine and cabergoline - cardiac valvulopathy
123
Name an MAO-B inhibitor
ORAL SELEGILINE or ORAL RASAGILINE
124
How do MAO-B inhibitors work
Inhibit MAO-B which breakdown dopamine = reduction of dopamine breakdown so dopamine remains for longer
125
Side-Effect of MAO-B inhibitor
Postural hypotension and AF
126
Name a COMT inhibitor
1. ORAL ENTACAPONE or TOLCAPONE
127
Role of COT inhibitr
Breaks down dopamine
128
Side-effect of COMT inhibitor
TOLCAPONe causes liver damage
129
Ho do we treat neuropsychiatric complications
ORAL CITALOPRAM = SSRIs | 2. ORAL QUETIAPINE (anti-psychotics)
130
Surgical treatments of Parkinson's
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)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions