neuro Flashcards
(150 cards)
1
Q
bells palsy pathophysiology
A
idiopathic UNILATERAL seventh cranial nerve palsy
lower motor neuron lesion (cranial nerve) so NO sparing of the forehead)
: we don’t know the cause, HSV (viral infection with HSV) HAS BEEN SUGGESTED AS one of the causes but its not fully understood
2
Q
bell’s palsy presentation
A
unilateral facial droop and loss in movement and sensation in that side of face
postauricular pain
hyperacusia
(these are due to 7th cranial nerve innervation of stapedius muscle which moderates the sound coming into ear- dampens it)
change in taste (since 7th innervates anterior 2/3 of tongue)
dry eyes
3
Q
bells palsy management
A
a lot of propositions have been made but consensus now is give oral prednisolone within 72 hours of presentation
antiviral ONLLY if severe but its effectiveness is questioned
eye care!!! to prevent exposure keratopathy give artificial tears and eye lubricants
4
Q
steps if no improvement of bells palsy in 3 week follow-up from presentation
A
refer urgently to ENT
5
Q
what referral do you do if bells palsy persists for months?
A
plastics
6
Q
prognosis of bells palsy?
A
most people recover within 3-4 months
15% may get some permanent moderate-severe weakness
7
Q
what is a TIA
A
its an interruption to the brains blood supply that resolves spontaneously within 24 HOURS (in reality most TIAs last about an hour)
8
Q
causes of ischaemic stroke
A
embolic (from heart eg AF) and thrombotic eg from carotids
risk factors are the typical cardiovascular risk factors
9
Q
cause of haemorrhagic stroke
A
can be spontaneous or elicited by trauma
most common is spontaneous due to berry aneurism that ruptures-
10
Q
presentation of stroke
A
BE FAST
balance
eyes
face
arms
speech
TIME- act fast
11
Q
classification system of stroke presentation
A
oxford classification system - classifies stroke into circulations: TOTAL anterior, Partial anterior circ (aka middle cerebral artery, Lacunar and posterior circulation
symptoms for anterior circulation:
1) eyes 2) face/ limb prob 3) speech prob
A) if you have all 3: TOTAL anterior circulation stroke?
B) if you have 2/3 its partial anterior circulation stroke aka middle cerebral artery (usually speech + body)
C) lacunar strokes
strokes in SUBCORTICAL areas: internal capsule, thalamus and basal ganglia
presents either as sensory contralateral stroke isolated
or motor contralateral isolated
OR BOTH of the above together but (NEVER SPEECH INVOLVED)
D) POSTERIOR circulation strokes
- loss of consciousness
- brainstem/ cerebellar syndromes
- or isolated homonymous hemianopia (posterior cerebral artery)
12
Q
ok oxford classification system sure but how should i actually remember the classification of strokes into the broad brain parts
A
1) CORTICAL strokes: anterior cerebral artery, middle cerebral artery (= anterior circulation) posterior cerebral artery (posterior circulation)
2) subcortical strokes: loss of sensation and movement or only on ein contralateral body but NOT SPEECH
3) BRAINSTEM/ cerebellar strokes WHEN THERE ARE CROSSED FINDINGS aka ipsilateral face symptoms and contralateral body symptoms
13
Q
how to classify brainstem strokes
A
1) midbrain, pons, medulla by thinking of cranial nerves in each part: 3+4, 5-8, 9-12
2) medial and lateral: generally Medial more Motor stuff and Lateral more Sensory
14
Q
what is weber syndrome
A
MEDIAL MIDBRAIN - IPSILATERAL occulomotor nerve palsy and contralateral limb
need to think weber-3
15
Q
what is locked in syndrome
A
a basilar circulation stroke, really bad, you are completely paralysed and maybe can communicate by blinking and eye movement + you are aware of what is happening
16
Q
what syndrome has facial asymetry
A
way to work thorugh it:
motor or sensory?- motor so medial
what cranial nerve? face so facial so 7 so pons
medial pontine syndrome - in basillar artery – remember branches of the BASE lead to problems in the FACE
17
Q
how does lateral pontine syndrome present?
A
characteristic is the SENSORY facial nerve problems so no sensation in face and anterior 2/3 of tongue
rememeber f-AIC-i-A-l
anterior inferior cerebellar artery
18
Q
lateral medullary syndrome
A
speech and swallowing difficulties and horners syndrome
PICA chew
Posterior inferior cerebellar artery
19
Q
medial medullary syndrome
A
think many Ms- mcdonalds - tongue wasting towards lesion (hypoglosal nerve- cranial nerve 9)
and motor on contralateral
anterior spinal artery –
20
Q
What potentially “ TIA- mimicking” differentials need to be excluded when investigating a TIA?
A
hypoglycaemia
Haemorrhage
21
Q
when a TIA is suspected what needs to be done if there are haemorrhage risk factors such as anticoagulation
A
URGENT referral for imaging to exclude haemorrhage eg CT head
22
Q
what first steps should be taken when a patient with suspected TIA is assessed?
A
immediately give aspirin 300mg and
referral to stroke specialist within 24 HOURS
23
Q
what does the stroke specialist need to do to investigate a TIA
A
MRI (including diffusion-weighted and blood-sensitive sequences) is preferred to determine the territory of ischaemia, or to detect haemorrhage or alternative pathologies
it should be done on the same day as the specialist assessment if possible
24
Q
what is the management of TIA for the weeks/ long term after event
A
DAPT - dual antiplatelet regime followed if not contraindicated
initially aspirin and clopidogrel for 21 days (bc higher risk during that time)
after 21 days only clopidogrel for secondary prevention
PPI also needs to be considered with DAPT
LONG TERM lipid modification with a statin is also considered but its not urgent like the anticoagulation
25
what is given if DAPT is not appropriate in TIA management
only clopidogrel
(and the statin)
26
what other investigation is done in SOME patients with TIA
CAROTID artery ultrasound - DUPLEX USS to see if stenosed, endarterectomy only if > 50% stenosis-- NASCET criteria, only if patient is not disabled
27
difference between a doppler and a dupplex ultrasound
doppler you listen to the blood through the vessel
dupplex you SEE the vessels on the black and white little screen
28
management of stroke acutely!
Exclude hypoglycaemia
Immediate CT brain to exclude haemorrhage
Aspirin 300mg daily for two weeks (started after haemorrhage is excluded with a CT)
Admission to a specialist stroke centre
29
MANAGEMENT of stroke in a patient that has been admitted in the stroke ward
1) thrombolysis with alteplase - once haemorrhage is excluded - post CT and ideally within 4.5 hours of symptom onset
2) CONsideration of thrombectomy alongside IV thrombolysis depending on the LOCATION of stroke
3) blood pressure should NOT be lowered unless there is a hypertensive crisis (needs to be below 185/ 110 for thrombolysis) but its generally dangerous to lower it- its VERY important in HAEMORHAGIc strokes
30
what strokes are eligible for thrombectomy
PROXIMAL anterior and PROXIMAL posterior circulation strokes
31
what are the two top underlying causes that are always investigated in stroke patients and how
AF and carotid artery stenosis with
Carotid imaging (e.g., carotid ultrasound, or CT or MRI angiogram)
ECG or ambulatory ECG monitoring
32
secondary prevention of stroke meaning management post discharge long term
Clopidogrel 75mg once daily (alternatively aspirin plus dipyridamole)
Atorvastatin 20-80mg (not started immediately – usually delayed at least 48 hours)
Blood pressure and diabetes control
Addressing modifiable risk factors (e.g., smoking, obesity and exercise)
33
trigeminal neuralgia presentation
intense facial pain in one of the divisions of the trigeminal nerve
can be described as stabbing shooting or like electricity
elicited by touch, shaving, cold, eating
90% UNILATERAL
may get progressively worse
can last from seconds to hours
34
patients with which condition are more likely to get trigeminal neuralgia?
multiple sclerosis
35
first line medication to treat trigeminal neuralgia
carbamazepine and various other things are possible if persistent symptoms
36
when someone has presented with a "blackout" or "collapse" and you suspect epilepsy what are features that support that
tongue bitting
convulsions obv
urinary incontinence
postictal phase of drowsiness and tiredness for about 15 mins
37
what are some other causes of seizures that are not epilepsy
febrile convulsions in children 0.5-5 years
alcohol withdrawal seizures
psychogenic non epileptic seizures
38
main classification features of seizures
1) location in brain
2) level of awareness during seizure
3) other things that happened before after or during seizure
39
categorise all types of seizures
focal- focal aware or focal impaired awareness and awareness unknown
also classified as motor (jacksonian march) or non motor or having aura etc
generalised
loss of consciousness always +from the start
motor: tonic clonic, tonic, clonic, myoclonic, atonic
typical absence : non motor
unknown onset seizures (dont know if it started focal or general bc no one was there or smth)
focal to bilateral seizure
40
investigations done for epilepsy
EEG and MRI
41
seizures that have sodium valporate first line for men and the alternative for women
generalised tonic clonic -levetiracetam or lamotrigine for women
Myoclonic- levetiracetaM for women
tonic and atonic - lamotrigine for women
42
focal seizures treatment
lamotrigine or levetiracetam both men and women
43
absence seizures treatment
ethosuximide
44
sodium valporate mechanism and side effectrs
ncreasing the activity of gamma-aminobutyric acid (GABA), which has a calming effect on the brain. Notable side effects include:
Teratogenic (harmful in pregnancy)
Liver damage and hepatitis
Hair loss
Tremor
Reduce fertility
45
status epilepticus definition
either:
A seizure lasting more than 5 minutes
Multiple seizures without regaining consciousness in the interim
46
management of status epilepticus
ABC:
- airway adjunct
- oxygen
- check blood glucose
First-line drugs are benzodiazepines
- in the prehospital setting PR diazepam or buccal midazolam may be given
- in hospital IV lorazepam is generally used. This may be repeated once after 5-10minutes
If ongoing (or 'established') status it is appropriate to start a second-line agent such as levetiracetam, phenytoin or sodium valproate
NICE state: levetiracetam quicker to administer and fewer adverse effects
'
If no response ('refractory status') within 45 minutes from onset, then the best way to achieve rapid control of seizure activity is induction of general anaesthesia or phenobarbital
47
presentation of acute subdural haemorrhage
CT findings:
presses on the brain
shifts midline
blood looks BRIGHT on the CT
caused by head trauma
SYMptoms can range from asymptomatic to focal neurological def to raised ICP symptoms to comma and coning
48
presentation of chornic subdural haemorrhage
more in older patients
blood dried in there
darker look in CT
may not recall specific trauma
can have cognitive changes, behavioural, neurological ect
49
categorise symptoms for all subdural haemorrhage types
Neurological Symptoms:
Altered Mental Status: Ranging from mild confusion to deep coma. Fluctuations in the level of consciousness are common.
Focal Neurological Deficits: Weakness on one side of the body, aphasia, or visual field defects, depending on the haematoma's location.
Headache: Often localised to one side, worsening over time.
Seizures: May occur, particularly in acute or expanding hematomas.
Physical Examination Findings:
Papilloedema: Indicates raised intracranial pressure.
Pupil Changes: Unilateral dilated pupil, especially on the side of the haematoma, indicating compression of the third cranial nerve.
Gait Abnormalities: Including ataxia or weakness in one leg.
Hemiparesis or Hemiplegia: Reflecting the mass effect and midline shift.
Behavioural and Cognitive Changes:
Memory Loss: Especially in chronic SDH.
Personality Changes: Irritability, apathy, or depression.
Cognitive Impairment: Difficulty with attention, problem-solving, and other executive functions.
Other Associated Features:
Nausea and Vomiting: Secondary to increased intracranial pressure.
Drowsiness: Progressing to stupor and coma in severe cases.
Signs of Increased Intracranial Pressure: Such as bradycardia, hypertension, and respiratory irregularities (Cushing's triad).
50
investigations for suspected acute subdural haemorrhage
head ct with contrast
51
management of acute subdural haemorrhage
Small or incidental acute subdurals can be observed conservatively. Surgical options include monitoring of intracranial pressure and decompressive craniectomy.
52
difference of chronic subdurals compared to acute on CT
On CT imaging they similarly are crescentic in shape, not restricted by suture lines and compress the brain ('mass effect').
In contrast to acute subdurals, chronic subdurals are hypodense (dark) compared to the substance of the brain.
53
MANAGEMENT of chronic subdurals
If the chronic subdural is an incidental finding or if it is small in size with no associated neurological deficit then it can be managed conservatively with the hope that it will dissolve with time.
If the patient is confused, has an associated neurological deficit or has severe imaging findings then surgical decompression with burr holes is required.
54
presentation/ possible symptoms of multiple sclerosis
- lethargy 75% of people and other non specific symptoms are common
basically someone with neurological symptoms, it really depends on where the demyelination of neurones is occuring-
common to cause optic neuritis so that can be a presentation
- spastic weakness most common in legs
- cerebellar: ataxia: more often in acute relapse
-tremor
urinary incontinence, sexual dysfunction, intellectual deterioraiton
sensory stuff -
55
types of MS
relapsing- remitting disease when you have periods of worsening of symptoms (last 1-2 months) followed by periods of remission
primary progressive disease - no relapsing remitting nature, illness is progressive from the start, less common but more likely amongst older people
secondary progressive disease - patients who had relapsing remitting disease who go on to develop secondary progressive disease within 15 yrs of diagnosis (65% OF REL rem patients get this)
56
multiple sclerosis investigations
i think conduction studies are normal or smth?
episodes need to be distributed in time and location
proof of this is either seperate lesions in brain MRI or seperate episodes in time
57
at what ages and gender is multiple sclerosis most commonly diagnosed in
people aged 20-40 years
3 times more common in women
much more common at higher latitudes
58
multiple sclerosis management aim
Treatment in multiple sclerosis is focused on reducing the frequency and duration of relapses. There is no cure.
59
management of acute relapse of multiple sclerosis
High-dose steroids (e.g. oral or IV methylprednisolone) for 5 days to shorten relapse (but doesnt change how well you will recover)
60
disease modifying drugs in MS when are they indicated
when 2 relapses in the past 2 years, and able to walk 10 m unaided for progressive and 100m for relaps/ remit.
61
disease modifying drugs in MS
natalizumab
ocrelizumab
fingolimod
beta interferon
glatiramer acetate
62
management of spasticity in multiple sclerosis
baclofen (muscle relaxant) and gabapentin (antiepileptic)
63
oscillopsia management of MS
GABAPENTIN IS first line
64
meningitis vs encephalitis presentation
meningitis has the neck stiffness headache fever photophobia (especially in bacterial meningitis)
encephalitis no fever, yes headache?
65
meningitis most common cause per age group
up to 3 months its smth - group b strep
3 months - 6 years its n. meningtitides
and till 60 years
and then > 60 its s. pneumoniae
66
suspected meningitis management in community
give iM benzylpenicillin and send to A+E
67
meningitis investigations in hospital
blood cultures LP unless contraindicated?
MRI?
68
viral vs bacterial vs tb meningitis LP findings
1) viral 2) bacterial 3) TB
glucose: 1- normal 2- low 3- low
protein: 1-HIGH 2- high 3- HIGH
opening pressure 1- normal 2- normal or high 3- normal
white blood cells 1- elevated: lymphocytes 2- very elevated: neuts and polymorphs 3- elevated lymph
appearance-1- clear/ cloudy 2- cloudy 3- cloudy SPIDER WEB
69
how much compared to plasma glucose does glucose in the CSF need to be considered low
< 50%
70
what is the most common meningitis and which is the most serious
viral most common bacterial more serious
71
parkinsons disease pathophysiology
progressive neurodegeneration of dopaminergic neurons in the substantia nigra
72
epidimeology of parkinsons: age and gender
males and peak at 65 yo
73
parkinsons disease presentation
classic triad of bradykinesia, tremor and rigidity
74
explain what bradykinesia entails in parkinson's
slow initiation of movement
poverty of movement; HYPOKINESIA
and slow shuffling steps with DECREASED arm swinging
75
explain tremor in parkinsons
resting tremor- so it improves with voluntary movement
pill rolling so between index and thumb
worse when stressed or tired
76
explain rigidity in parkinsons
rigidity generally means resistance to the passive movement of a limb
lead pipe rigidity - so feeling a constant stiffness when dr trying to move their limb
cogwheel is when it feels like granazi- start stop - because of combination of rigidity and the tremor
77
other potential symptoms of parkinsons other than the triad
REM sleep cycle syndrome
psychiatric and most commonly depression - other : dementia
masked like facies
flexed posture
micrographia
drooling of saliva
impaired olfaction
autonomic dysfunctions such as postural ypotension
78
how can you tell the difference between parkinsons and drug induced parkinsonism
motor symptoms are rapid onset and BILATERAL in parkinsoNISM! vs classically assymetrical in parkinsons!
rigidity and rest tremor are uncommon in parkinsonism
79
how is parkinsons diagnosis usually made and what can be done if there is difficulty differentiating essential tremor and parkinsons?
usually clinical diagnosis but can also do a SPECT
80
what is the management of parkinsons
needs management by an specialist in movement disorders
we should know however just because its common to come across
if the symptoms affecting quality of life then levodopa
if not then can chose between dopamine agonists, levodopa or Monoamine Oxidase B inhibitor (MAO-B)
81
which parkinsons medication leads to comparatively most DALY and motor symptoms improvement when used as first line?
LEVODOPA
82
which parkinsons medication has least specified side effects but more motor complications
levodopa
83
what are some of the specified side effects from parkinsons medications
hallucinations
impulse control disorders
excessive sleepiness
84
which Parkinsons medication can most commonly cause impulse control disorders
dopamine agonist therapy and more common with history of alcohol consumption or smoking or impulsive behaviors
85
what is noRmal ICP
7-15mmHg in adults in the supine position
86
what is the Cerebral perfusion pressure? (calculation)
CCP is the net pressure gradient causing cerebral blood flow to the brain
CCP= Mean Arterial Pressure- ICP
87
Causes of ICP
- idiopathic intracranial hypertension
- traumatic head injuries
- infection
- meningitis
- tumours
- hydrocephalus
88
features of ICP
- headache
- vomiting
- reduced levels of consciousness
- papilloedema
- Cushing's triad:
1) widening pulse pressure
2) bradycardia
3) irregular breathing
89
Investigations used in ICP to investigate the underlying cause?
neuroimaging (CT/MRI) is key to investigate the underlying cause
90
ICP invasive monitoring aims and options
- catheter placed into the lateral ventricles of the brain to monitor the pressure
- may also be used to collect CSF samples and also to drain small amounts of CSF to reduce the pressure
- a cut-off of > 20 mmHg is often used to determine if further treatment is needed to reduce the ICP
91
management principles of raised ICP
- investigate and treat the underlying cause
- head elevation to 30º
- IV mannitol may be used as an osmotic diuretic
- controlled hyperventilation
- removal of CSF, different techniques include:
92
HOW does controlled hyperventilation work to lower ICP, purpose and cautions
- aim is to reduce pCO2 → vasoconstriction of the cerebral arteries (increased co2 leads to vasodilation since body wants to washout the excess CO2 so it increases blood flow so opposite happens in reduced co2- constriction)
→ reduced ICP
leads to RAPID, TEMPORARY lowering of ICP. However, CAUTION needed as may reduce blood flow to already ischaemic parts of the brain
93
what nerve injury leads to wrist drop
radial nerve
94
causes of radial nerve damage
humeral shaft fracture, crutches
95
nerve injury presenting with hand of benediction
median nerve injury: BENEDICTION: CANNOTBEND the index and middle finger!!! dont confuse with ulnar claw hand see other card
96
what nerve injury leads to claw hand
ulnar nerve, cannot extend the little and eing fingers!!! dont confuse with hand of benediction where the OTHER fingers cannot bend!!!!
97
what nerve can be damaged in shoulder dislocation or a surgical neck fracture and what is the result clinically
axillary nerve, leads to flat shoulder
98
what nerve injury leads to foot drop
sciatic nerve
99
what things can cause sciatic nerve injury
hip dislocation and IM injection
100
when do you see steppage gait (person walking and lifting knee and hip higher to step)
common peroneal nerve injury
101
when is the person not able to tiptoe
tibital nerve injury
102
nerve palsy causing Ptosis, "down and out" eye, pupil ± involved
occulomotor nerve: diabetes, aneurism, herniation
103
nerve palsy causing vertical diplopia
CN IV (Trochlear)
vertical-- so it means worse when looking down so worse when going down stairs
Trauma
104
horizontal diplopia nerve palsy
abducents (VI)
Raised ICP, MS
105
Facial numbness, jaw deviation, absent corneal reflex
cn 5 TRIGEMINAL
V1: Herpes zoster, V3: Jaw weakness, corneal reflex
106
cranial nerve palsy causing Hearing loss, vertigo, nystagmus
CN VIII (Vestibulocochlear)
causes:
Acoustic neuroma, labyrinthiti
107
Dysphagia, hoarse voice, uvula deviation
CN IX/X (Glossopharyngeal/Vagus) Stroke, bulbar palsy
108
Weak shoulder shrug, head turning
nerve palsy?
CN XI (Accessory) Iatrogenic (neck surgery)
109
Tongue deviation (toward lesion), fasciculations nerve palsy?
CN XII (Hypoglossal) Stroke, MND
110
what is the pathology behind horners syndrome
The sympathetic supply to the eye and face
This is not a cranial nerve, but a 3-neuron sympathetic pathway from the hypothalamus to the eye
111
what is the triad involved in horners syndrome
Ptosis – drooping of the upper eyelid (mild)
Miosis – constricted pupil
Anhidrosis – loss of sweating on the face/forehead (same side)
112
important causes of Horner's syndrome
1) Central (1st-order):
-- Brainstem stroke (lateral medullary/Wallenberg syndrome)
---Demyelination (e.g. MS)
2) Preganglionic (2nd-order):
-- Pancoast tumor (apical lung cancer)
-- Neck surgery/trauma
3) Postganglionic (3rd-order):
-- Carotid artery dissection (painful Horner’s!)
-- Cavernous sinus pathology
-- Cluster headache (episodic Horner’s)
113
what is a radiculopathy
Radiculopathy is a condition caused by compression, inflammation, or injury to a nerve root.
This is where the nerve exits the spinal cord and enters the peripheral nervous system.
114
common causes of radiculopathies
herniated discs (MOST COMMON for cervical and lumbar radiculopathy) , spinal stenosis, tumors, trauma, or infection.
115
common symptoms of radiculopathies
Radiculopathies can affect both motor and sensory functions, leading to a variety of symptoms like pain, weakness, and sensory changes.
116
which nerve root radiculopathy is it when theres Shoulder weakness, biceps weakness, numbness in the deltoid
C5 root compression
117
which nerve root radiculopathy is it when theres Radial forearm pain, thumb weakness, loss of biceps reflex.
C6
118
which nerve root radiculopathy is it when theres Weakness in dorsiflexion of the foot (foot drop), sensory loss over the lateral leg and dorsum of the foot.
L5
119
which nerve root radiculopathy is it when theres Weakness in plantar flexion (tiptoe walking), sensory loss over the posterior leg and sole of the foot, loss of Achilles reflex.
S1
120
which nerve root radiculopathy is it when theres Triceps weakness, pain radiates down the arm to the middle finger, loss of triceps reflex.
C7
121
cauda equina syndrome what is it and why important
Rare, but a medical emergency that occurs when multiple lumbar and sacral nerve roots are compressed.
Symptoms: Bowel/bladder dysfunction, saddle anesthesia, severe lower back pain, leg weakness.
Immediate surgical decompression
122
what is the straight leg raise test or sciatic nerve stretch test and what does a positive test look like and indicate
when examiner lifts your leg extended
positive: Reproduction of the patient’s sciatic-type pain (shooting pain, tingling, or burning) radiating below the knee, often into the calf or foot.
Indicates L5 or S1 nerve root irritation (commonly due to disc herniation).
123
what is the femoral stretch test
patient lies prone so face down and knee flexed and you pull it up so thigh lifts from bed
positive is when Reproduction of pain (typically burning, sharp, or tingling) in the:
Anterior thigh
Sometimes the groin or medial leg
It suggests lumbar radiculopathy at L2–L4, often due to:
Disc herniation (especially at L3–L4)
124
first line management of sciatica- dermatome associated/ lower back pain
similar to that of other musculoskeletal lower back pain: analgesia, physiotherapy, exercises:
NICE recommend using the same drugs as for back pain without sciatica symptoms i.e. first-line is NSAIDs +/- proton pump inhibitors rather than using neuropathic analgesia (e.g. duloxetine)
125
when do you further investigate sciatica- dermatome associated/ lower back pain and what investigation
if symptoms persist e.g. after 4-6 weeks on conservative/ pain management) then referral for consideration of MRI is appropriate
126
what are indications for urgent MRI in sciatica/ back pain
anything that looks like cauda equina
bladder problems: dont feel fullness, dont feel urge to empty, incontinence bad!
saddle paresthesia (perianal pins and needles ect)
leg weakness
BILATERAL sciatica bc usually its on one side
127
what MMSE score suggests dementia
128
what are features that are characteristic of delirium and not dementia
more acute
also IMPAIRED CONSCIOUSNESS (not present in dementia)
129
features of alzheimers
Amnesia (recent memories lost first)
Aphasia (word-finding problems, speech muddled and disjointed)
Agnosia (recognition problems)
Apraxia (inability to carry out skilled tasks despite normal motor function)
130
second most common cause of dementia after alzheimers and third
vascular
lewy body dementia
131
what is a characteristic feature in presentation of symptoms in vascular dementia
Can have a 'step-wise' progression due to progressive infarcts over time
132
vascular dementia diagnosis
Usually a clinical diagnosis. Neuro-imaging can show evidence of significant small vessel disease
133
which condition is lewy body dementia related to and in what ways
parkinsons since the pathophysiology in both involves the abnormal protein deposits: lewy bodies in different parts of the brain
also in terms of symptoms, lewy body dementia can present with parkinsonism (rigidity, tremor, bradykinesia)
134
when is a diagnosis of parkinsons made vs lewy body dementia when both motor and cognitive symptoms arise?
typically occurs before parkinsonism, but usually both features occur within a year of each other.
This is in contrast to Parkinson's disease, where the motor symptoms typically present at least one year before cognitive symptoms
IF WITHIN THE YEAR regardless of order: dementia
if MORE THAN A YEAR apart: parkinsons
135
what type of visula hallucinations is common in lewy body dementia
liliputian: little people, little animals ect
136
what is a later feature in fronto temporal dementia compared to other types
memory loss is a late feature
137
three main variants of fronto temporal dementia
Behavioural variant (60%), characterised by loss of social skills, personal conduct awareness, disinhibition, and repetitive behaviour.
Semantic dementia (20%), characterised by an inability to remember words for things, calling them 'thingy.'
Progressive non fluent aphasia (20%), where the patient can't verbalise; their speech is laboured and difficult.
138
what is an epidemiological dif or frontotemporal dementia compared to other types and a risk factor
Classically presents at a younger age than other forms of dementia, and risk factors include repetitive head injury
139
diagnostic proccess of dementia?
Functional history (which may require a collateral history, risk assessment)
Cognitive assessments
Brain imaging
140
examples of cognitive tests used for dementia assessments
MMSE, MOCA, 10-point Cognitive Screener (10-CS), 6-item Cognitive Impairment Test (6-CIT), 6-item Screener, Memory Impairment Screen (MIS), Mini-Cog, Test Your Memory (TYM).
141
blood tests done in presentation of suspected dementia
confusion screen and is often done in primary care. It includes FBC, U&E, LFTs, CRP/ESR, Ca2+, TFTs, B12, folate, syphilis, HIV.
142
dementia management steps once reversible causes have been excluded
refer to a specialist dementia diagnostic service (such as a memory clinic or community old age psychiatry service. Here, a full functional assessment is carried out and the patient will be referred for neuroimaging, such as CT or MRI.
143
what aspects are important in the risk assessment of dementia patients?
HOW SAFE?:
HOme safety (gas)
Wandering
Self neglect
Abuse
Falls
Eating
144
mild/ moderate altzheimers medication
donepezil
145
severe altzheimers medication
memantine
146
medication for lewy body dementia
acetylcholinesterase inhibitors
147
main management in vascular dementia
optimising CV profile in VD.
148
Behavioural and psychological symptoms in dementia medication
low-dose risperidone
149
what medication class is CONTRAINDICATED in behavioural and psychological dementia symptoms?
antipsychotics!!!
associated with increased stroke and VTE in the elderly, and are contraindicated in Lewy Body Dementia and Parkinsons Disease.
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