Neurology Flashcards
1
Q
Types of stroke
A
Ischemic- clots
Haemorrhagic- bleeds
TIA (transient ischemic attack
2
Q
Which is more common ischaemic or haemorrhagic stroke
A
Ischaemic stroke-85%
Haemorrhagic- 15%
3
Q
Ischaemic Stroke
A
Interruption of cerebral blood supply:
Embolism
Thrombosis
Systemic hypoperfusion
4
Q
Stroke- FAST
A
FACE
ARMS
SPEECH
TIME TO CALL 999
5
Q
Anterior cerebral artery supplies
A
midline portions of the frontal lobe and parietal lobe
6
Q
Middle cerebral artery supplies
A
majority of the lateral surface of the hemisphere
7
Q
Posterior cerebral artery supplies
A
inferior portion of the temporal lobe and occipital lobe
8
Q
Wernicke area
A
Controls the ability to understand the meaning of words
9
Q
Broca’s area
A
premotor area for speech sounds
10
Q
Wernicke’s area location
A
Usually found on left superior temporal gyrus
11
Q
Broca’s area location
A
Left posterior inferior frontal gyrus
12
Q
Wernicke’s area blood supply
A
Inferior division of the MCA
13
Q
Broca’s area blood supply
A
Superior division of the MCA
14
Q
Oxford Community Stroke Project (OCSP) Classification
A
Clinical classification of patterns of neurological deficit in acute ischaemic stroke
15
Q
Oxford Community Stroke Project (OCSP) Classification- different classifications
A
Anterior Circulation Infarction- Partial (PACI) or Total (TACI)
Posterior Circulation Infarction (POCI)
Lacunar Infarction (LACI)
16
Q
Anterior Circulation Infarction- arteries affected
A
Anterior and middle cerebral arteries
17
Q
Anterior Circulation Infarction- signs and symptoms
A
Contralateral weakness
Contralateral sensory loss/sensory inattention
Dysarthria
Dysphasia (receptive, expressive)
Homonymous Hemianopia/visual inattention
Higher cortical dysfunction
18
Q
Posterior Circulation Infarction- arteries affected
A
2 vertebral arteries, basilar artery, 2 posterior cerebral arteries
19
Q
Posterior Circulation Infarction- signs and symptoms
A
Cranial nerve palsy and a contralateral motor/sensory deficit (‘crossed signs’)
Conjugate eye movement disorder (e.g. horizontal gaze palsy)
Cerebellar dysfunction (e.g. vertigo, nystagmus, ataxia, dysarthria)
Isolated homonymous hemianopia
Bilateral events can cause reduced GCS
20
Q
Lacunar Infarction
A
Occlusion of deep penetrating arteries
Affects a small volume of subcortical white matter
Underlying process is often referred to as small vessel disease
21
Q
Lacunar Infarction- symptoms
A
Do not present with cortical features as subcortical white matter affected e.g. dysphasia, apraxia, neglect, visual field loss
22
Q
Lacunar syndromes
A
Pure motor hemiparesis
Ataxic hemiparesis
‘Clumsy hand’ and dysarthria
Pure hemisensory
Mixed sensorimotor
23
Q
Total anterior circulation stroke (TACS)- criteria
A
All 3: Unilateral weakness, homonymous hemiopia, higher cerebral dysfunction
24
Q
A
25
26
Partial anterior circulation stroke (PACS)- criteria
2 of: Unilateral weakness, homonymous hemiopia, higher cerebral dysfunction
27
28
Lacunar syndrome (LACS)
1 of: Pure sensory stroke, pure motor stroke, sensori-motor stroke, ataxic hemiparesis
29
30
Posterior circulation syndrome (POCS)
1 of: Cranial nerve palsy + contralateral motor/ sensory deficit, bilateral motor/sensory deficit, conjugate eye movement disorder, cerebellar dysfunction, Isolated homonymous hemiopia or cortical blindness
31
32
NIHSS- NIH Stroke Scale
Grade and track the severity
Monitor response to acute treatments
33
34
Stroke- 1st line investigation
Urgent CT Head (+/- CT angiography)
35
36
Stroke- Head CT purpose
Differentiae between ischemic and haemorrhagic stroke
37
Utility of CT in acute stroke- pros
Quick
Readily available 24/7
Sensitive for haemorrhage
May see a ‘hyperdense vessel’
38
Utility of CT in acute stroke- cons
Cannot usually diagnose an infarct in the acute phase
Less sensitive than MRI for picking up other abnormalities, LACS + PCS
39
ASPECTS- Alberta Stroke Program Early CT Score
Segmental estimation of early infarction on CT head in MCA stroke
RAPID software uses a machine learning algorithm to calculate this score.
40
Ischemic Stroke- treatment-Thrombolysis
Breaks down acute clot- potentially life saving
Within 4,5 hrs of symptoms on set
Risk- haemorrhage, allergic reaction
41
Ischemic Stroke- treatment-Thrombolysis- Contraindications
Symptoms only minor/ rapidly improving
Haemorrhage on CT/MRI
Active bleeding from any site
Recent GI/UT haemorrhage
Recent treatment with heparin/warfarin
Recent surgery/trauma
Plus many more
42
Post-thrombolysis care
More aggressive blood pressure monitoring
Vigilance for complications (bleeding)
24 hour CT head (haemorrhagic transformation)
43
Mechanical Thrombectomy
Mechanical recanalisation of the culprit vessel (catheter aspiration and/or stent retrievers)
6 hour time-window
44
Mechanical Thrombectomy- risk
femoral haematoma/ pseudoaneurysm, retroperitoneal bleeding, vessel rupture, arterial dissection
45
Ischaemic Penumbra
Reversibly injured brain tissue around ischemic core (irreversibly damaged brain tissue)
46
Pathological subtypes of ischaemic stroke (TOAST classification)
Large vessel disease (50%)
Small vessel disease (25%)
Cardioembolic (20%)
Unknown (cryptogenic) (3%)
Rare causes (2%) e.g. dissection, CVST, vasculitis
47
Stroke- treatment- lifestyle
Smoking cessation
Drug and alcohol cessation
Dietary modifications
Exercise
Driving advice
48
Stroke- treatment- medical
Thrombolysis
Antiplatelet
Anticoagulation
Statin therapy
49
Stroke- treatment
Thrombolysis +/- Mechanical Thrombectomy if indicated
or Aspirin 300mg
50
Neuroepithelial cells
stem cells that differentiate into neurons and glial cells
51
Glia (gilal cells or neuroglia)
non-neuronal cells in the CNS (brain and spinal cord) and the peripheral nervous system that do not produce electrical impulses.
They maintain homeostasis, form myelin, and provide support and protection for neurons.
52
Types of Glial cells
Astrocytes, ependymal cells, oligodendrocytes, microglial
53
Astrocytes
perform metabolic, structural, homeostatic, and neuroprotective tasks
54
Oligodendrocytes
produce the myelin sheath insulating neuronal axons
55
Gliomas
a common type of brain tumour, include astrocytoma, ependymoma, oligodendrocyte
WHO grade 1 and 2 – “low”
WHO grade 3 and 4 – “high”
56
Germ cell tumours
rare paediatric usually cancerous tumours in the pituitary/pineal region
57
Tumour of the sellar region
Craniopharyngiomas a usually benign, cystic tumours
58
Brain tumours- cranial nerves
Schwannoma e.g. eighth nerve - acoustic neuroma
59
Brain tumour- Haematopoietic
Lymph cells - primary CNS lymphoma
60
Brain tumour- Secondary /metastatic tumours
Lung
Breast
Colorectal
Testicular
Renal cell
Malignant melanoma
61
Brain tumour- WHO classification
Graded according to how fast they grow and how likely they are to grow back after treatment using both histology and genetics into four grades of malignancy
-1 most benign, 4 most malignant
62
Brain Tumour Grades 1
Slow growing, non-malignant, and associated with long-term survival
63
Brain Tumour Grades 2
Have cytological atypia. These tumours are slow growing but recur as higher-grade tumours.
64
Brain Tumour Grades 3
Have anaplasia and mitotic activity. These tumours are malignant
65
Brain Tumour Grades 4
Anaplasia, mitotic activity with microvascular proliferation, and/or necrosis. These tumours reproduce rapidly and are very aggressive malignant tumours
66
Low grade gliomas – grade 2
Slow growing but will undergo anaplastic transformation
Astrocytomas – 3-5 years
Oligodendroglioma – 7-10 years
Average Survival 10 years
Median age 35 years
67
High Grade Gliomas – 3 and 4
Most common type - 85% of all new cases of malignant primary brain tumour
Either as primary tumour or from pre-existing low grade
68
High Grade Gliomas – 3 and 4- natural history
Median age onset 45 for 3, 60 for 4
Survival times 3 – 3-5 years 4 – 12 months
69
Brain tumour- known causes
Majority no cause found
Ionising radiation
5% family history
Immunosuppression (CNS lymphoma)
70
Brain tumour- symptoms
Varied- dependent on tumour type, grade and site
-Headache
-Seizures
-Focal neurological symptoms
-Other non-focal symptoms
71
Brain tumour- headache
Woken by headache, worse in the morning, worse lying down, associated with N&V, exacerbated by coughing, sneezing, drowsiness
Typically 1st symptom and seen at presentation
72
Headache- brain tumour vs norm pop
70% patients with brain tumour will have headache (same as normal population)
73
Brain tumour- headache red flags
Headache PLUS
Headache and age (>50)
New/changed headache
Previous history of cancer
74
Frontal lobe function
Prefrontal area – Personality, Inhibition
Frontal - Motor function, Language production (Broca’s area)
75
Parietal lobe function
Sensory processing
Spatial orientation
Visual field pathway
76
Occipital lobe function
Visual processing
77
Cerebellum function
Balance, coordination
78
Temporal lobe function
Language comprehension
Auditory processing
Visual field pathway
Memory
79
Brainstem function
cranial nerve nuclei
control subconscious body functions
80
Focal symptoms
(progressive over days – weeks)
Weakness
Sensory loss
Visual/speech disturbance
Ataxia
81
Non-focal symptoms
Personality change/behaviour
Memory disturbance
Confusion
82
Brain tumour- seizures
21% presenting symptom
>80% patients with a brain tumour
First fit 2-6% = brain tumour
83
Frontal lobe- seizure
Limb jerking, head or eye deviation
84
Parietal lobe- seizure
Sensory disturbance – spreading tingling
85
Occipital lobe- seizure
Positive visual disturbance - coloured balls
86
Temporal lobe- seizure
Déjà vu
Jamais vu
Memories
Feeling of dread
Rising feeling
87
Seizure- signs
Papilloedema-
Focal neurological deficit- Hemiparesis, Hemisensory loss, Visual field defect, Dysphasia
88
Papilloedema
Swelling of the optic disc due to elevated intracranial pressure
89
Low grade brain tumour- presentation
typically present with seizures (can be incidental finding)
90
High grade brain tumour- presentation
rapidly progressive neurological deficit. Symptoms of raised intracranial pressure
91
Brain tumour- headache red flags
- With features of raised intracranial pressure (including papilloedema and VIth nerve palsy)
-With focal neurology. Check for field defect
92
Brain tumour- urgent referrals
New onset focal seizure
Rapidly progressive focal neurology (without headache)
Past history of other cancer
93
Brain tumour- 1st line investigations
Imaging- CT (with contrast), MRI
Functional MRI
94
Brain tumour- 2nd line investigation
Brain biopsy/surgery- Histology, molecular markers and genetics
95
Brain tumour- treatment
Depends on tumour type, grade and site
Treatment is non-curative (except for grade I)
96
Brain tumour prognosis
Brain cancer 5 year survival rate is 12%
Compare to breast cancer – 76% over 10 years
97
Brain tumour- treatment high grade glioma
Steroids, surgery, chemo
Radiotherapy is mainstay of treatment
98
Brain tumour- treatment low grade glioma
Surgery – early resection
Radiotherapy and early chemotherapy
99
Traumatic brain injury
Evidence of neurological dysfunction caused by external force
100
Traumatic brain injury- aetiology
RTC, falls (elderly), assaults, sports and recreation
101
Contrecoup injury
Counterblow, brain lies in CSF, collision on head causes "free floating" brain to head back of head
102
Primary vs secondary Traumatic brain injury
primary brain injury results from mechanical injury at the time of the trauma
secondary brain injury is caused by the physiologic responses to the initial injury
103
Contusions
Bruising of the brain, close to bony providences
104
Diffuse axonal injury
White matter lesions, high rotation or deceleration
Little haemorrhage- need MRI to see
105
Types of brain haemorrhage
epidural haemorrhage, subdural haemorrhage, subarachnoid haemorrhage, and intraparenchymal haemorrhage
106
Epidural haemorrhage
Most dangerous but if drained, good recovery
bleeding between the inside of the skull and dura mater
107
Subdural haemorrhage
Presents typically with milder trauma
Collection of blood under the dura mater
108
Subarachnoid haemorrhage
Can cause finger like extensions of blood that fill the sulci and bathe the brain as seen on CT
Accumulation of blood between the arachnoid and pia mater
109
Intraparenchymal haemorrhage
bleeding into the brain parenchyma proper
110
Secondary traumatic brain injury- treatment
Maintenance of homeostasis- (iv fluids, glucose ect)
Management of seizures- diazepam
Surgery- rarer
111
When to CT- presents with a head injury
Any form of clinical concern- not returned to pretty much near normal when under observations
112
Glasgow coma scale
Composed of three parameters: best eye response (E), best verbal response (V), and best motor response (M), 3-15, 3 being the worst and 15 the best
113
Chronic traumatic encephalopathy
Only found at autopsy
Thought to be linked to repeated head injuries and blows to the head
114
Basal ganglia disease
Hardware problem and software problems (no cell dead, problem with brain circuit)
115
Basal ganglia disease- hardware problems
Parkinson’s disease
Huntington’s disease
116
Basal ganglia disease- software problems
Essential tremor
Dystonia
Tourette
117
Parkinson's disease- three cardinal features
Brady/Akinesia- (problems with buttons, writing smaller, walking deteriorated)
Tremor- (at rest, may be unilateral)
Rigidity
118
Spasticity vs rigidity
Spasticity- more resistance in one direction, more tone initial part of movement, velocity dependent
Rigidity- Same resistance in all directions, not velocity dependent
119
Spasticity vs rigidity- pathophysiology
spasticity arises as a result of damage to the corticoreticulospinal (pyramidal) tracts, rigidity is caused by dysfunction of extrapyramidal pathways
120
Bradykinesia
slowness of movement and speed (or progressive hesitations/halts) as movements are continued
121
Akinesia
inability to perform a clinically perceivable movement
122
Parkinson's disease- aetiology
Cell loss in substantia nigra- Inherited factors, oxidative stress, mitochondrial dysfunction, environmental factors (risk factors, toxin induced)
123
Parkinson's disease- pathophysiology
Loss of dopaminergic neurons in the substantia nigra
124
Parkinson's disease- treatment overview
Non curative, to replace lost dopamine to reduce symptoms
125
Parkinson's disease- treatment- L dopa
L-dopa > dopamine> dopamine receptor
126
Parkinson's disease- treatment- dopamine agonist
Activate dopamine receptor like dopamine
127
Parkinson's disease- treatment- COMT/MAO-B inhibitors
Inhibits Catechol-O-Methyl-Transferase + Monoamino-
oxidase- reponisble for removing the neurotransmitters norepinephrine, serotonin and dopamine from the brain
128
Parkinson's and tremor on action
Unlikely to be Parkinson's, more likely to be essential tremor
129
Essential tremor- signs
Postural/action tremor
No/little rest tremor
No increased tone
No problems with fine finger movements
130
Essential tremor- treatment
BBs, primidone
Deep brain stimulation useful
131
Essential tremor-pathophysiology
Software issue- the result of an abnormally functioning central oscillator
132
Meningitis
Inflammation of the meninges
133
Meninges
Outermost- dura mater
Arachnoid
Pia Mater
134
Causes of Meningitis- infective
Bacterial
Viral
Fungal
Parasitic
135
Causes of Meningitis- non infective
Paraneoplastic
Drug side effects
Autoimmune (e.g. vasculitis/SLE
136
Meningitis- infective routes
Via blood stream
Extracranial infection
Neurosurgical complications
137
Meningitis- infective- pathophysiology
Bacteria enter CSF, either transcellularly (through endothelial cells) or paracellularly (next to endothelial cells)
Infected WBCs can act as trojan horse
138
Meningitis- infective barriers
Blood-CSF and blood-brain barrier ordinarily protect against meningitis and encephalitis respectively
139
Infective meningitis- classic triad
fever, headache, neck stiffness
140
Infective meningitis- first line antibiotic in community
IM benzylpenicillin
141
Infective meningitis- 1st line investigations
Assess GCS (Glasgow Coma Score)
Blood cultures
142
Infective meningitis- 1st line treatment
Broad spectrum antibiotics
Steroids (IV dexamethasone)
143
Infective meningitis- first line antibiotic in hospital
ceftriaxone or cefotaxime
144
Infective meningitis- first line antibiotic- special considerations
Penicillin allergic
Immunocompromised 🡪 risk of listeria
Recent travel 🡪 risk of penicillin resistance
145
Infective meningitis- diagnostic investigation
Lumbar puncture and lab tests
146
Infective meningitis- gram Negative cocci
Neisseria
147
Infective meningitis- gram positive cocci
Pneumococcus (strep.pneumoniae)
148
Infective meningitis- bacterial clinical signs
May appear septic
Focal neurology
?purpuric rash
149
Infective meningitis- viral clinical signs
Recent viral illness
Less severe
150
Infective meningitis- TB clinical signs
Weight loss
Night sweats
Insidious onset
151
Infective meningitis- cryptococcal clinical signs
HIGH OPENING PRESSURE!!!- when doing lumbar puncture
152
Infective meningitis- bacterial RFs
Students
Travel
Immunosuppressed
153
Infective meningitis- Viral RFs
Small children
Immunosuppressed
154
Infective meningitis- TB RFs
TB contact
Immunosuppressed
155
Infective meningitis- cryptococcal RFs
HIV
Immunosuppressed
156
Infective meningitis- bacteria species- neonate
Strep B
157
Infective meningitis- bacteria species- child
N. meningitidis, S. pneumoniae,
*H. Influence*
158
Infective meningitis- bacteria species- adult
*Neisseria* meningitidis, S. pneumoniae
159
Infective meningitis- bacteria species- elderly
N. meningitidis, *S. pneumoniae*
160
Infective meningitis- bacteria species- immunocompromised
Listeria
161
Encephalitis- causes
Usually viral
-Herpes Simplex
-Varicella Zoster
Tropical
Non-infective- autoimmune, paraneoplastic
162
Encephalitis
Inflammation of the brain
163
Encephalitis- signs
Preceding “flu-like” illness
Altered GCS: confusion, drowsiness, coma
Fever
Seizures
Memory loss
(+/- meningism)
164
Encephalitis- investigations
MRI head
Lumbar puncture (Lymphocytic CSF, Viral PCR)
165
Encephalitis- treatment
Mostly supportive
Aciclovir if HSV or VZV
166
Tetanus
Inoculation through skin with Clostridium tetani spores (found globally in soil)
e.g. stepping on a nail, dirty wounds
Bacteria produce toxins!
167
Tetanospasmin
travel retrogradely along axons
Interferes with neurotransmitter release 🡪 increased neuron firing 🡪 unopposed muscle contraction and spasm
Incubation around 8 days
168
Tetanus- management
Vaccinate if risk injury
Supportive- Muscle relaxants
Paracetamol/cooling
Immunoglobulin to mop up toxin
Metronidazole to clear any residual bacteria
169
Rabies
Virus- Inoculation through skin with saliva of rabid animal (dogs, cats, foxes etc)
e.g. lick, bite, splash
Travels retrogradely along nerves
170
Stroke
a clinical syndrome, caused by cerebral infarction or
haemorrhage, typified by rapidly developing signs of focal and global disturbance of
cerebral functions lasting more than 24 hours or leading to death
171
Transient ischemic attack (TIA)
acute loss of cerebral or ocular
function with symptoms lasting less than 24 hours caused by an inadequate
cerebral or ocular blood supply as a result of low blood flow, ischemia, or embolism
associated with disease of the blood vessels, heart or blood
172
Ischemic stroke- aetiology
Blood vessel in the brain is blocked
Usually, an atherosclerotic plaque or a clot in a larger artery ruptures, travels
downstream, gets trapped in a narrower artery in the brain.
Embolic strokes are common complications of AF and atherosclerosis of
the carotid arteries
173
Haemorrhagic stroke- aetiology
Bleeding from a blood vessel within the brain.
HTN is the main cause of intracerebral haemorrhagic stroke.
174
Strokes- Differential Diagnosis
Hypoglycaemia Labyrinthine disorders
Migrainous aura
Mass lesions
Postictal weakness
Simple partial seizures
Functional hemiparesis
175
ABCD2 Score
estimates risk of stroke (CVA) after a transient ischemic attack (TIA)
176
ABCD2 Score- stands for
Age: >60yrs (1 point)
BP >140/90 (1 point)
Clinical features
-Unilateral weakness, 2 points
-Speech disturbance without weakness, 1 point.
Duration (60 mins< = 2 points, 10–59 mins =1 point)
Diabetes (1 point)
177
High risk of TIA becoming stroke
ABCD2 >3
Or AF, 1< TIA in a week, TIA on anticoagulants
178
TIA treatment
Low risk < 7 days, high risk <1 day
Statin, antiplatelet (clopidogrel or aspirin), treat BP, no driving until seen by a specialist
179
Active Rehabilitation
Facilitating recovery through modification of the neural networks
180
Active Rehabilitation techniques- Priming
Makes NS more receptive to rehabilitation interventions: Imagery, Touch, Transcranial direct current stimulation, Transcranial magnetic stimulation
181
Active Rehabilitation techniques-Augmenting
Augment the effects of rehabilitation interventions- Robotics, Biofeedback
182
Active Rehabilitation techniques- Specific interventions
Neurophysiological
Task Specific practice
183
Adaptation
Incomplete Recovery- strategies facilitate recovery of function through training, use of aids and appliances or modification of environment
184
Preventative rehabilitation
Reduce immobilisation: Passive range of motion exercises
185
Gait in neurological disorders
Weakness
Balance
Stiffness
Slowness
186
Walking
Heelstroke, footflat, midstance, pushoff, acceleration, midswing, deceleration
187
Dropped foot
Inability to activate ankle dorsiflexors in swing phase of gait
188
Dropped foot- pathophysiology
Lesion of CNS- corticospinal tract
189
Balance treatment
Vestibular exercises
Physiotherapy
Increase the base
Improve vision
190
Posture and slow treatment
Dopaminergic drugs
Metronomes
191
Spasticity
Disordered sensori-motor control resulting from an UMN lesion, presenting as intermittent or sustained involuntary activation of muscles
192
Headache classification- Primary
Migraine, Cluster, Tension Type
193
Headache classification- Secondary
Meningitis, Subarachnoid Haemorrhage, GCA, Idiopathic Intracranial Hypertension, Medication overuse headache
194
Brain tumour- headache red flags
New headache with Hx cancer, Cluster headache, Seizure, Significantly altered conciousness, memory, confusion, coordination, Papilloedema
195
Kernig's sign
Pts is kept in supine position, hip and knee are flexed to a right angle, and then knee is slowly extended- resistance or pain >135 degree= +ive kernig sign
196
Positive Kernig's sign
Meningitis
197
Migraine signs
Attacks last 4-72 hours
Two of the following: Unilateral , Pulsing, Moderate/severe, Aggravation by routine physical activity
Nausea and /or vomiting
Photophobia and phonophobia
198
Photophobia
abnormal sensitivity to light, especially of the eyes
199
Phonophobia
persistent, abnormal, and unwarranted fear of sound
200
Migraine pain
Unilateral, pulsing, Moderate/severe, Aggravation by routine physical activity
201
Tension type headache signs
30 mins to 7 days
Bilateral
Pressing/tightening (non pulsating) quality
Mild or moderate intensity
Not aggravated by routine physical activity
No nausea or vomiting (anorexia may occur)
No more than one of photophobia and phonophobia
202
Tension type headache- characteristic
Bilateral
Pressing/tightening (non pulsating) quality
Mild or moderate intensity
Not aggravated by routine physical activity
203
Cluster headache
Severe or very severe unilateral orbital, supraorbital and/or temporal pain lasting 15-180
minutes if untreated
Accompanied by ipsilateral cranial autonomic features +/ a sense of
restlessness or agitation
Attacks have a frequency from 1 every other day to 8 per day
204
Cluster headache- pain
Severe or very severe unilateral orbital, supraorbital and/or temporal pain lasting 15-180 mins
205
Trigeminal Neuralgia- definition
intense facial pain in the distribution of the trigeminal nerve
206
Classical Trigeminal Neuralgia
distributions of the trigeminal nerve
Electric shock like, shooting, stabbing or sharp
Precipitated by innoculous stimuli to the affected side of the face
207
Migraine- acute treatment
Oral triptan + NSAID/ paracetamol
DO NOT USE OPIOIDS
208
Migraine- preventive treatment 1st line
topiramate or propranolol
209
Migraine- preventive treatment 2nd line
Amitriptyline
210
Meningitis signs
Drowsy, Pyrexial, Neck stiffness
211
Subarachnoid Haemorrhage signs
Thunderclap headache – max severity within seconds
212
Subarachnoid Haemorrhage- 1st line investigations
CT head
213
Subarachnoid Haemorrhage- management
Surgery for aneurysms
Nimodipine- CCB to prevent vasospasm
214
Raised Intracranial Pressure signs
Worse on waking, coughing, sneezing, straining, lying down (postural)
Nausea, vomiting
Papilloedema
215
Papilloedema
swelling of the optic disc due to elevated intracranial pressure
216
Idiopathic Intracranial Hypertension signs
Headache of raised ICP
Visual disturbance – acuity, fields
Papilloedema
217
Idiopathic Intracranial Hypertension RFs
Obesity
Drugs (tetracycline)
Female
218
Idiopathic Intracranial Hypertension investigations
CSF normal but pressure high
Imaging to exclude secondary cause and cerebral venous sinus thrombosis
219
Idiopathic Intracranial Hypertension management
Management of RFs (ie wgt loss)
consider pharmacotherapy
220
Idiopathic Intracranial Hypertension- pharmacotherapy
Acetazolamide / Topiramate/ Diuretics
221
Giant Cell Arteritis (GCA)
>50 yrs
Associated with PMR
Jaw claudication
Visual symptoms
Tender temporal arteries
Raised inflammatory markers
222
Giant Cell Arteritis (GCA) diagnostic investigation
ultrasonography +/ temporal artery biopsy
223
Giant Cell Arteritis (GCA) 1st line treatment
high dose steroid
224
Chronic Daily Headache
Headache on ≥ 15 days per month
225
Chronic headache- common primary causes
*Chronic Migraine*, Tension-type headache, cluster headache, paroxysmal hemicranias
Hemicrania continua
New daily persistent headache
226
Chronic headache- common secondary causes
*Medication overuse headache*
Chronic post-traumatic headache
Raised intracranial pressure
Low CSF pressure headache
Chronic meningitis
227
Medication overuse headache- common causes
Ergotamine, Triptans, Opioids or Combination analgesic medications
228
Medication overuse headache
Regular use for >3 months of one or more symptomatic treatment
Headache has developed or markedly worsened during drug use
229
Dystonia
Prolonged muscle contraction causing abnormal posture or related movements
230
Idiopathic generalized dystonia
Childhood-onset dystonia often starting in 1 leg with ipsilateral progression
Genetic cause is common
231
Focal dystonia
Dystonia confined to one part of the body
232
Focal dystonia- examples
Spasmodic torticollis, blepharospasm, writer cramp
233
Spasmodic torticollis
head pulled to one side
234
Blepharospasm
involuntary contraction of orbicularis oculi (responsible for closing eyelids)
235
Acute dystonia
Medication induced dystonia
236
Acute dystonia- examples
Torticollis (head pulled back), trismus (oromandibular spasm) +/ oculogyric crisis (eyes drawn back)
237
Acute dystonia- treatment
diphenhydramine or benzatropine- antidopaminergic agents
238
Generalised dystonia- treatment
Levodopa + physio
239
Focal dystonia- treatment
botulinum toxin + physio
240
Tourette syndrome
complex neurodevelopmental disorder characterised by motor and vocal tics beginning in childhood
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Tourette syndrome- RFs
Male, 3-8 yrs, PMH/FH of OCD or ADHD, FM of tourette's
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Tourette syndrome- pathophysiology
Unknown, multiple genetic loci implicated and neuroanatomical differences on MRI
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Tourette syndrome- tic paradox
Tics are voluntary, but often unwanted- the desire to tic comes from the relief of the odd sensation that builds up prior
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Tourette syndrome- non medical treatment
Cognitive behavioural approaches- 1st line
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Tourette syndrome- medical treatment
Alpha-2 agonist, antipsychotic, botox
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Epilepsy- differential diagnosis
Postural syncope, hypoglycaemia, migraine, Benign paroxysmal Positional vertigo, TIA, cardiogenic syndrome
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Epileptic Seizure
Paroxysmal event in which changes of behaviour, sensation and cognition are caused by excessive, hypersynchronous neuronal discharges in the brain
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Epileptic Seizures- characteristics
30-120 seconds
May occur from sleep
Stereotypical seizures / syndromal seizure types
May be associated with other brain dysfunction
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Epileptic Seizures- temporal lobe
Focal impaired awareness seizure
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Epileptic Seizures- Frontal lobe
Focal aware seizure
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Focal seizure
Originating within networks linked to one hemisphere + often seen with underlying structural disease
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Focal seizure without impairment of consciousness
Awareness is unimpaired with focal, motor, sensory, automimic or psychic symptoms
No post-ictal symptoms
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Focal seizure with impairment of consciousness
Awareness is impaired- either at seizure onset or following a simple partial aura
Commonly temporal lobe- post ictal symptoms is a feature
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Focal seizure evolving into a bilateral, convulsive seizure
2/3 pts with partial seizures, electrical disturbances start focally, spreads widely, causing generalized seizure, typically convulsive
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Generalized seizures
Originating at some point within an rapidly engaging bilaterally distributed networks leading to simultaneous onset of widespread electrical discharge with no localizing features (to one hemisphere)
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Absence seizures
Brief pauses eg suddenly stops talking mid sentence, then carries off where they left off, presents in childhood
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Tonic-clonic seizures
Loss of conscience, limbs stiffen (tonic) then jerk (clonic)- may have one without the other
Post-ictal confusion + drowsiness
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Myoclonic seizures
sudden jerk of a limb, face or trunk
Pts may be thrown to ground or have a violently disobedient limb- 'flying saucer epilepsy'
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Atonic (akinetic) seizures
Sudden loss of muscle tone causing a fall, no LOC
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Syncope
Paroxysmal event in which changes in behaviour, sensation and cognition are caused by an insufficient blood or oxygen supply to the brain.
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Syncope- characteristics
Situational
Typically from sitting/ standing- rarely sleep
Duration 5-30 seconds- recovery in 30s
Presyncopal symptoms
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Cardiogenic syncope- characteristics
less warning, history of heart disease
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Functional / dissociative (nonepileptic) seizure
Paroxysmal event in which changes in behaviour, sensation and cognition are caused by mental processes triggered by internal or external aversive stimuli.
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Functional / dissociative (nonepileptic) seizure- characteristics
Situational
Duration 1-20 minutes
Dramatic motor phenomena or prolonged atonia, Eyes closed, Ictal crying and speaking
Rapid or slow postictal recovery
History of psychiatric illness, other somatoform disorders
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Epilepsy versus syncope: Factors suggestive of epilepsy
Tongue biting, head turning, muscle pain, cyanosis (blue/grey lips), postictal confusion
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Epilepsy versus syncope: Factors suggestive of syncope
Prolonged upright position, sweating prior to LOC, nausea, presyncopal symptoms (dizzy, nausea, sweating, palpitations), pallor
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Epilepsy vs. Functional / Dissociative Seizures- suggestive of FDS
Very frequent, prolonged attacks
Those in which the body movements come and go
Attacks where the person is emotionally upset afterwards
Pre-ictal anxiety
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Structural / metabolic (focal) epilepsy
Associated with focal brain abnormality, may start at any age
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Structural / metabolic (focal) epilepsy- types of seizures
Partial seizures +/- with impairment of consciousness, secondary generalised seizures
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Structural / metabolic (focal) epilepsy- first line treatment
Lamotrigine (anticonvulsant)/ carbamazepine (anticonvulsants)/ levetiracetam (anticonvulsants)
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Structural / metabolic (focal) epilepsy- first line investigation
MRI- anatomical temporal lobe abnormalities
EEG can be diagnostic but a normal EEG does not exclude epilepsy
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Genetic (idiopathic) generalised epilepsy
No associated brain abnormality, manifestation usually <30 years
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Genetic (idiopathic) generalised epilepsy- seizure types
Absence, myoclonic, primary generalised tonic clonic seizures
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Genetic (idiopathic) generalised epilepsy- first line treatment
Lamotrigine (anticonvulsant) / levetiracetam (anticonvulsant)/ valproate (anticonvulsant)
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Genetic (idiopathic) generalised epilepsy- diagnostic test
EEC- electroencephalogram
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Modes of action of Anti-seizure medications- presynaptic neurone
Inhibit voltage-gated Na+/ Ca2+
Increase activity of voltage-gated K+
Inhibit SV2A
Overall decrease in pre-synaptic excitability and neurotransmitter release
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Modes of action of Anti-seizure medications- inhibitory neurotransmitters
Increase activity of GABA receptor
Inhibit GABA transaminase/ transporter
Overall more GABA in synapse
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Modes of action of Anti-seizure medications- presynaptic neurone- Voltage gated Na+ channels
Na+ influx increases excitability and drives APs
Inhibited by carbamazepine, lamotrigine, oxcarbazepine
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Modes of action of Anti-seizure medications- presynaptic neurone- Voltage gated K+ channels
K+ efflux reduces neuronal excitability, channel activity increased
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Modes of action of Anti-seizure medications- presynaptic neurone- Voltage gated Ca2+ channels
Ca2+ influx drives neurotransmitter release, channel inhibited
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Modes of action of Anti-seizure medications- presynaptic neurone- SV2A
Requires for release of neurotransmitter from vesicles
Inhibited by levetiracetam
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Modes of action of Anti-seizure medications- inhibitory neurotransmitters- target the GABA receptor
Reduces neuronal excitability
GABA receptor activity increased by benzodiazepines, barbiturates, felbamate, topiramate
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Modes of action of Anti-seizure medications- inhibitory neurotransmitters- target the GABA transaminase
Degrades GABA, inhibited to elevate GABA levels
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Modes of action of Anti-seizure medications- inhibitory neurotransmitters- target the GABA transporter
Removes GABA from the synapse, inhibited to elevate GABA levels
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Other epilepsy therapies
Surgery
Vagus nerve simulation
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Cerebellum anatomy
largest part of the hindbrain, located in posterior cranial fossa
comprises of two hemispheres joined by the vermis- sub-divided into three lobes – anterior, posterior, and flocculonodular separated by two transverse fissures
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Role of the cerebellum- main
accuracy and coordination
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Role of the cerebellum
-accuracy and coordination
-motor control and learning
-contributes to timing and sensory acquisition
-involved in the prediction of the sensor consequences of action
-eye movements, speech, limb movements, fine motor skills, gait, posture,
balance, cognition
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Ataxia
Sign, not a disease + results from cerebellar dysfunction (problems with balance and co-ordination) can be caused by structural damage to the cerebellum or can be inherited or acquired
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Ataxia- aetiology
Inherited- autosomal dominant, autosomal recessive (Friedreich’s ataxia), X linked, mitochondrial
Acquired- toxic/metabolic (alcohol, vit def, drugs), immune mediated (gluten related) infective, degenerative, trauma, neoplastic
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Symptoms of cerebellar dysfunction
-dizzy – unsteady / wobbly / clumsy
-falls, stumbles
-difficulty focusing / double vision / ‘oscillopsia’
-slurred speech
-problems with swallowing
-tremor
-problems with dexterity / fine motor skill
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Nystagmus
rhythmical, repetitive and involuntary movement of the eyes
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Ataxia- clinical signs
Gait is unsteady with a tendency to falls
Hand coordination is impaired
Dysarthria or dysphagia may be present
Ocular symptoms- nystagmus
Intentional tremor
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Classification of ataxia
Scale for the Assessment and Rating of Ataxia (SARA)
Mild- mobilising independently or with one walking aid
Moderate- Mobilising with 2 walking aids or walking frame
Severe- predominantly wheelchair dependent
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Ataxia-first line investigation
MRI brain demonstrates cerebellar atrophy and / or dysfunction
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Ataxia- common blood test
For genetic testing, autoimmune screen (esp gluten related serology)
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Motor neurone disease (MND)
Cluster of neurodegenerative disease characterised by selective loss of neurone in motor cortex, cranial nerve nuclei, and anterior horn cells
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Motor neurone disease (MND) vs MS and polyneuropathies
Never sensory loss or sphincter disturbance in MND, unlike MS and polyneuropathies
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Motor neurone disease (MND) vs myasthenia
MND never affects eye movement, distinguishing from myasthenia
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Motor neurone disease (MND)- 4 types
ALS (amyotrophic lateral sclerosis or Lou Gehrig’s disease)- most common
Progressive bulbar palsy- 10-20%
Progressive muscular atrophy <10%
Primary lateral sclerosis- rare
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ALS (amyotrophic lateral sclerosis)
Loss of motor neurones in motor cortex + anterior horn of the cord, so combined UMN + LMN signs
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UMN symptoms
Weakness (pyramidal)
Spasticity
Hyperreflexia
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LMN symptoms
Wasting
Weakness
Fasiculation
Hypotonia/flaccidity
Reflexes are reduced
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Progressive bulbar palsy
disease of the nuclei of CN IX-XII
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Progressive bulbar palsy- signs
Progressive, relentless
Oropharyngeal muscles
Dysarthria
Dysphasia
Jaw spasms/bruxism
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Progressive muscular atrophy
Anterior horn cell lesion, so LMN signs only
Affects distal muscles groups before proximal
Better prognosis than ALS
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Primary lateral sclerosis
Loss of betz cells in motor cortex
Mainly UMN, marked leg spastic leg weakness and pseudobulbar palsy, no cognitive sign
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Motor neurone disease- investigations
Clinical diagnosis
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Motor neurone disease- treatment overview
Improve survival and QoL
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Motor neurone disease- treatment
Riluzole
Non-invasive ventilation- for Nocturnal respiratory insufficiency
Multi-disciplinary specialist care
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Motor neurone disease- treatment- riluzole
inhibitor of glutamate release and NMDA receptor antagonist
Only medication to improve survival
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Dementia
A neurodegenerative disease with progressive decline in several cognitive domains
20% of pop > 80 yrs
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Dementia subtypes
Alzheimer's disease, vascular dementia, Lewy body dementia, frontotemporal dementia
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Alzheimer's disease
Most common type of dementia, cognitive impairment is progressive, non-cognitive symptoms may come and go, but pts become sedentary
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Alzheimer's disease risk factors
1st degree relative, Down's syndrome, genetics, low physical/ cognitive activity, depression, loneliness, smoking
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Alzheimer's disease pathophysiology
Atrophy in the temporal, frontal and parietal area
Senile plaques (beta-amyloid) and neurofibrillary tangles are the characteristic histopathological features postmortem
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