Neuro Flashcards
1
Q
what differentiates between stroke and TIA?
A
Stroke, symptoms lasting for > 24 hours
TIA, symptoms lasting < 24 hours
2
Q
what is crescendo TIA
A
> 2 TIA in 1 week
3
Q
aetiology of ischaemic infarction
A
small vessel occlusion or thrombosis in situ
cardiac emboli –> AF, endocarditis
atherothoromboembolism eg carotids
vasculitis
4
Q
aetiology of haemorrhagic infarction
A
CNS bleeding –> HTN, ruptured aneurysm, anticoagulation, thrombolysis
5
Q
what are some rapid recognition screening tools which can be used to identify stroke
A
in primary care - FAST - face, arm, speech, test (any focal neuro loss)
in ER - ROSIER
6
Q
what are the different types of stroke according to oxford/Bamford classification for ischaemic stroke
A
total anterior circulation syndrome
Partial anterior circualtion syndrome
Posterior circulation syndrome
Lacunar syndrome
7
Q
what are the criteria for total anterior circulation syndrome
A
must have all 3
1) unilateral weakness +/- a sensory deficit of face, arm or leg
2) homonymous hemianopia
3) high cognitive unction - dysphagia, visuospatial disorder
8
Q
what are the criteria for partial anterior circulation syndrome
A
must have 2
1) unilateral weakness +/- a sensory deficit of face, arm or leg
2) homonymous hemianopia
3) high cognitive unction - dysphagia, visuospatial disorder
9
Q
what are the criteria for posterior circulation syndrome
A
1 of the following:
cerebellar or brainsteam syndrome - Webner’s syndrome etc
Cranial nerve palsy and a contralateral motor/sensory deficit
Bilateral motor/sensory deficit
loss of consciousness
isolated homonymous hemianopia
Conjugate eye movement disorder – gaze palsy
Cerebellar dysfunction – ataxia, nystagmus, vertigo
10
Q
clinical features of TIA
A
• Suspect TIA if sudden onset focal neurological deficit which has completely resolved within 24 hrs Unilateral weakness or sensory loss. Dysphasia. Ataxia, vertigo, or incoordination. Syncope. Sudden transient loss of vision in one eye (amaurosis fugax). Homonymous hemianopia. Cranial nerve defects.
11
Q
clinical features of stroke
A
o Weakness − sudden loss of strength in the face or limbs.
o Sensory loss – paraesthesia or numbness.
o Speech problems such as dysarthria.
o Visual problems – normally homonymous hemianopsia
o Dizziness, vertigo or loss of balance — isolated dizziness is not usually a symptom of TIA.
o Specific cranial nerve deficits such as unilateral tongue weakness or Horner’s syndrome (miosis, ptosis, and facial anhidrosis).
o Inattention/neglect
o Confusion, altered level of consciousness and coma.
o Difficulty with fine motor co-ordination and gait.
o Neck or facial pain (associated with arterial dissection).
o Initially flacid and no reflexes then Spasticity +/- clonus, ↑ tendon reflexes
o Weakness in extensors of arms and flexors of legs = hemiplegic gait – UMN lesion
o Posterior circulation strokes:
Acute, persistent continuous vertigo
Dizziness with nystagmus
N+V
Head motion intolerance
New gait unsteadiness
12
Q
what are the criteria for Lacunar syndrome
A
1 of the following
- unilateral weakness +/- sensory deficit of face and arm and leg or all 3
- pure sensory stroke
- ataxic hemiparesis
13
Q
what are some differentials for stroke
A
Bell’s palsy - don’t have forehead sparing
migraines - with aura, aura without headache etc
Metabolic causes - hypo/hypergycaemia, hypocalcemia
MS
epilepsy
blackouts/syncope
subdural haemorrhage (trauma-related)
14
Q
what are the criteria for immediate CT head (next available slot or within 1 hour)?
A
- indications for thrombolysis or early anticoagulation treatment
- on anticoagulant treatment/known bleeding tendency
- GCS < 13
- unexplained progressive or fluctuating symptoms
- papilloedema, neck stiffness or fever
- severe headache at onset of stroke symptoms
15
Q
what is the management of an ischaemic stroke
A
thrombolysis with altepase (IV) - within 4.5 hours of symptoms onset
CT head again at 24 hours after alteplase
aspirin 300mg from Day 2 for 2 weeks
SALT team involvement for swallowing assessment
early mobilisation
screen for malnutrition
16
Q
what happens if alteplase cannot be given
A
300mg aspirin for 2 weeks
17
Q
what specialist managements are there for stroke
A
maintenance or restoration of homeostasis
- O2 if stats < 95%
- BM between 4 -11
- IV insulin and glucose for DM pts
- antihypertensive therapy only in hypertensive emergency
- consider BP reduction to 185/110 to lower
18
Q
Pharmacological management of ischaemic stroke
A
aspirin 300mg for 2 weeks from alteplase then switch to clopidogrel 75mg long-term
statin - start 48 hours after alteplase if not already on it
warfarin/dabigatran if potential causes of cardiac thromboembolism (AF, prosthetic valves)
defer antihypertensive for 1-2 weeks as inc BP can be physiological
19
Q
what are some management for hemorrhagic stroke which can be carried by the neurosurgeons?
A
decompressive hemicraniectomy for MCA infarct
intracerebral haemorrhage - surgery for hydrocephalus, combination of prothrombin and Vit K in patients on anticoagulants
20
Q
definition of meningitis
A
viral or bacterial infection to the meninges of the brain
21
Q
what is the bacterial cause of meningitis in neonates
A
Listeria
Group B streptococcus
22
Q
what is the bacterial cause of meningitis in infants/young children
A
H.influenza
strep. pneumoniae
23
Q
what is the bacterial cause of meningitis in adult
A
strep. pneumoniae
Neisseria meningitis
24
Q
what are some viral causes of meningitis
A
herpes
enterovirus
varicella zoster
25
clinical features of meningitis in children and adult
headache
fever
N+V
photophobia
neck stiffness
altered consciousness - confusion
seizure
• focal neurological signs non-reactive pupil, abnor of ocular motility, abnor visual fields, gaze palsy, arm or leg drift
• non-blanching rash meningococcal meningitis
• Kernig’s sign – pain in lower back or back of thigh on extension of knee when hip is flexed at 90 degree
• Brudzinski’s sign – forced flexi of the neck elicit a reflex flexion of the hips
26
clinical features of meningitis in neonates and babies
non-specific signs and symptoms - hypotonia, poor feeding, lethargy, hypothermia, bulging fontanelle
27
investigation for meningitis
```
LP + blood culture (prior to abx)
blood glucose
pneumococcal and meningococcal PCR
FBC, U&E, CRP, LFT, Clotting, VBG
viral PCR
serum HIV
```
28
what does the lumbar puncture show if bacterial meningitis
```
cloudy appearance
inc protein
reduce glucose
inc WCC and neutrophils dominant
culture - usually +ve
```
29
what does the lumbar puncture show if viral meningitis
```
clear appearance
normal protein level
normal glucose level
inc WCC lymphocytes
usually can not be cultured
```
30
management of meningitis
if discovered in the community --> IV/IM benylpenicillin
< 1 year - 300mg
1-9 years - 600 mg
> 10 - 1200mg
if discover in the hospital
< 3 months - cefotaxime + amoxicillin (cover listeria contracted during pregnancy from mother)
> 3 months - ceftriaxone or cefotaxime
Dexamethasone for 4 days can help reduce inflammation and preserve hearing in children
• Single dose ciprofloxacin for close contact within 7 days prior to the onset of symptoms.
public health notifiable
31
what prophylaxis do you provide with those who had close contact with a patient who is confirmed to have bacterial meningitis
single-dose ciprofloxacin
32
what is another name for acute confusional state
delirium - alternating cognition with a fluctuating course
33
what is the ICD-10 definition for acute confusional state
Aetiology non-specific syndrome characterised by concurrent disturbances of consciousness and attention, perception, thinking, memory, psychomotor behaviour, emotion and the sleep-wake cycle (that is) transient and of fluctuating intensity.
34
causes of acute confusional state?
PINCH ME
```
pain
infection
nutririon/electrolyte imbalance/meatbolic disturbances
constipation
hydration
```
medications
environmental
35
RF for acute confusional state
* Age > 65
* Hospitalisation
* Dementia
* Frailty/multiple co-morbidities
* Significant injuries such as hip fracture
* Functional impairment (for example immobility and the use of physical restraint’s)
* Hx of /current excess alcohol use
* Sensory impairment
* Poor nutrition
* Lack of stimulation
* Terminal phase of illness
36
clinical features of acute confusional state
```
acute onset
fluctuating course (lucid interval during day and worse at night)
2 types - hypoactive/hyperactive
```
cognitive/consciousness - clouded, poor concentration, confusion, slow response, memory and language impairment
inattention - person is easily distractible and have difficulty focusing
disorganised thinking
perception - visual and auditory hallucination possible
physical
if hypoactive - more lethargic, reduced mobility, lack interest in daily activities, reduced appetite, become quiet and withdrawn
if hyperactive - increased sensitivity to their immediate surroundings with agitation, restlessness, sleep disturbance, and hyper-vigilance. Restlessness and wandering are common.
social - lack of co-operation with a reasonable request, withdrawal or alterations in communication, mood, and attitude
37
investigation for acute confusional state
initial screening - history (both patient and collateral hix to assess acute onset and fluctuating course)
assess cognition - AMTS
A-E assessment - full assessment looking for signs of infection and any other causes for deirium
confusion bloods- FBC, U&E, LFT, TFT, Ca2+, glucose, B12, folate, CRP/ESR, syphilis
urine dip +/- urine drug screen
review medication charts
38
management of acute confusional state
biological
- identify any underlying causes
- supportive management eg hydration, nutrition, address pain, restrict use of catheters
- antipsychotics or sedation in pt who are aggressive (haloperidol/olanzapine)
- Benzo for alcohol withdrawal (delirium tremens)
psychological
- Identify and treat reversible cause e.g. dementia.
- Supportive: safety, encourage engagement reminders of time, orientation, familiar objects/people, maintain a sleep-wake cycle, calm manner, avoid physical restraints, encourage them to walk.
social -
- Minimise change and moving of environment.
- Control environment e.g. single room, quiet.
- Control disruptive behaviours which may harm other patients
- No driving until delirium has resolved
39
definition of subarachnoid hemorrhage
bleeding into the subarachnoid space (between the pica and archnoid matter) --> usually result of ruptured cerebral aneurysm
40
aetiology of subarachnoid hemorrhage
rupture of berry aneurysm (circle of willis)
41
RF for subarchnoid haemorrhage
```
hypertesnion
smoking
excessive alcohol consumption
cocaine use
female
45-70 yrs old
black
FHx
sickle cell anaemia
Av malformation, coarctation of aorta
PCKD, ehlers danlos, marfans
neurofibromatosis
```
42
clinical features of subarchnoid haemorrhage
sudden onset thunderclap headache - occurs during strenuous activity eg exercise/sex
depressed/loss of consciousness
CN3 compression - eyelid dropping, diplopia with mydriasis, orbital pain
papilloedema, retinal bleed
meningism - stiff neck photophobia, N+V
+ve Kernig (extend leg pain) and Brudzinski (bow)
neuro signs - speech changes, weakness, seizures
43
investigation for subarachnoid hemorrhage
non-contrast CT head - if SAH - blood around the circle of willis ie starfish of death
FBC, U&E, LFT, Clotting, BM (hypoglycemia)
ECG - arrythmia, prolong QT, ST segement, tall T-wave
LP - if CT inconclusive & after 12 hours - red cell count high + xanthochromic, 3 samples needed
CT angiography - once confirmed SAH to look for bleeds location for fixation prep
44
management of SAH
A-E assessment, urgent referral to a specialist neurosurgical unit. monitor CNS, BP, pupils, GCS
anaesthetist if GCS < 8
fluid to inc cerebral perfusion (aim system > 160)
nimodipine (Ca antagonist) to dec vasospasm and cerebral ischaemia risk
dexamethason - dec cerebral oedema
analgesia and anetiemtics
antiepileptic - treat seizures
surgery to treat aneurysm - endovascular coiling, Stents, Ballon, clipping
45
what is the most common complications of SAH
hyponatremia - can lead to arrhythmia - cardiac arrest
46
definition of sub-dural haematoma
collection of blood between the dural and arachnoid covering of the brain
47
aetiology of sub-dural haematoma
* Most common cause = trauma (in both Acute and chronic)
* Rupture of a cerebral aneurysm (less common)
* Vascular malformation – AV malformation or dural fistula
* All of the above damage to the bridging vein leading to subdural bleeds
* Common in elderly and alcoholics
48
what are the different classification of subdural haematoma
* Acute < 3 days old, diffusely hyperdense
* Subacute 3-21 days old, heterogeneously hyperdense/isodense
* Chronic > 21 days, diffusely hypodense
* Acute-on-chronic areas of hyperdensity within hypodense haematoma
49
clinical feaures of subdural haematoma
* Physical signs of trauma
* Headache – inc intracranial pressure
* N+V – inc intracranial pressure
* Diminished eye response anisocoria (unequal pupil response, can be a sign of brainstem herniation)
* Reduced GCS
* Confusion
* LOC
* Seizures
* Loss of bowel and bladder continence
* Localised weakness
* Sensory changes
* Speech or vision changes
* Otorrhoea – basal skull fracture
* Rhinorrhoea – basal skull fracture
50
investigation for a subdural haematoma
non-contrast CT banana shaped (crescentic in shape and can cross suture line), density of the lesion = age of haematoma
* MRI scan can help to determine the degree of damage
* Plain skull X-ray possible skull fracture
51
Mx of acute sub-dural haematoma
If < 10 mm size, midline shift < 5mm non-expansile without significant neuro dysfunction
o Observation + monitoring (cerebral pressure monitoring)
o Prophylactic antiepileptics (7 days) phenyton or levetiracetam
o Correct any anticoagulant used eg warfrain
o Lower intracranial pressure bed head @ 30 degree, adequate analgesia and sedation, hyperosmolar therapy (to draw fluid back into serum), mannitol (osmotic diuretis)
If > 10 mm, midline shift > 5mm or expansile or significant neuro dysfunction
o Surgery what type of surgery depends on the location of the haematoma burr hole craniotomy, hemicraniectomy and duraplasty
o All of the other observation, monitoring, prophylactic antiepileptics, lower intracranial pressure
52
managment of chronic haematoma
* Antiepilictics – phenytoin, levetiracetam
* Elective surgery eg twist-drill craniotomy with coninuous catheter drainage
* Correction of coagulopathy
* Lowering intra-cranial pressure
53
definition of extra-dural haematoma
• Collecition of blood in the potential space between the dura and the bone. Can occur in the spinal column
54
aetiology of extra-dural haematoma
* Fracutred temporal or parietal bone damaging the middle meningeal artery or vein blood collecting between the dura and the skull
* Trauma to the temple
* Dural venous sinuses
* Can occur in the spinal olumn – after trauma of epidural anaesthesia or LP
55
clinical features of extra-dural hematoma
* Hx of trauma to the head
* A lucid period then rapid deterirations extra-time
* Headaches
* N+V
* Seizures
* Bradycardia +/- hypertension inc intracranial pressure
* CSF otorrhea or rhinorrhoea resulting from skull fracture with a tear of the dura
* Dec GCS
* Unequal pupils anisocoria
* Facial nerve injury
* Weakness of limbs
* Focial neuro deficit
56
investigation for extra-dural hematoma
Plain x-ray can show skull fracture
Cervical spine x-ray can see the spinal injury and must be excluded
Non-enhanced CT head lenticular shape (lemon) & & can not cross suture line repeat CT head if any deterioration
Bloods FBC, U&Es, coag, group & save
57
mx of extradural haematoma
If acute trauma A-E assessment
If subacute can be treated conservatively + supportive management
If intra-cranial pressure inc IV osmotic diuretics (mannitol), hypertonic saline, positioning of the patient
Large haematoma + unstable patient surgery eg burr holes
v.similar to sub-dural haematoma
58
definition of seziure
• A transient occurrence of signs and/or symptoms due to abnor excessive or synchronous neuronal activity in the brain’
• Defined by the following
At least 2 unprovoked (or reflex) seizures occurring >24 hours apart
1 unprovoked (or reflex) seizure and a probability of further seizures similar to the general recurrence (at least 60%) after 2 unprovoked seizures, occurring over the next 10 years
Diagnosis of an epilepsy syndrome
59
what are the different types of epilepsy?
general - motor
general - non-motor eg abscence
focal - being aware or impaired awareness
unknow onset
60
causes of epilepsy
```
anoxia
head injuries
brain tumors
infections - meningitis, encephalitis
stroke
metabolic abnor - eg hypoglycaemia
genetic and congenital malformations
```
61
definition of focal epilepsy
Electrical and clinical manifestations arise from one portion of the brain
62
what are the subtypes of focal epilepsy?
focal aware
focal impaired awareness
63
clinical features of focal seizures
Either focal aware or focal impaired awareness of seizure
Movement in one side of the body or one part of the body
Premonitory sensation or sequence of sensation more likely to indicate a focal seizures in temporal lobed fear, epigastric sensation, déjà vu, jamais vu)
Automatisms picking at clothes, smacking of the lips
Can develop into bilateral tonic-clonic epilepsy
Can have post-ictal focal neuro deficit Todd’s paralysis, aphasia
64
clinical features of generalized tonic clonic seizures
LOC with tonic (muscle tensing) and clonic (muscle jerking)
Associated tongue biting, incontinence, groaning, irregular breathing.
Post-ictal- confused, drowsy, irritable, depressed
65
clinical features of generalized atonic seizures
Indicative of lennox gastaut syndrome
Aka drop attacks
Brief lapses of muscle tone
Last around 3 minutes.
66
clinical features of generalized myoclonic seizures
Sudden brief muscle contraction like a “jump”
| Common in children as juvenile myoclonic epilepsy
67
clinical features of generalized infantile seizures
West syndrome
- 6 months - clusters of full body spasms
- might draw leg towards chest
68
clinical features of generalized absence seizures
common in children
patient becomes blank stares into space and abruptly return to normal
- lasting 10-20 seconds
- most stop having seizures at older ages
69
what are the investigations for epilepsy
• 1st seizure not Ix with EEG.
• EEG indicative after unprovoked seizures
o EEG- typical patterns in different forms of epilepsy
• Bloods BM, FBC, U&Es, urinary drug screen, LP and CSF analysis (evidence of infection)
• CT head – any structural/stroke
• MRI brain: structural abnormalities.
• Can do video/EEG long-term monitoring
70
management of generalised tonic clonic, atonic, myoclonic and absence epilepsy
1st line - sodium valporate
2nd line - lamotrigine
3rd line - dual therapy
avoid carbamazepine in myoclonic and absence - can exacerbate the symptoms
avoid sodium valproate in pregnancy, but can continue using it if other meds trailed and failed
71
management of focal epilepsy
1st line - carbamazepine
2nd line - sodium valproate
3rd line - dual therapy
4th line - surgery
72
how long do you have to stop driving if you have epilepsy
6 months if one-off seizure
| 1 year if multiple seizures
73
definition of status epilepticus
seizure klasting > 5 minutes or > 3 seizures in 1 hour
74
aetiology of status epilepticus
```
low AED dose
stroke
alcohol
withdrawal
anoxic brain injury
infection
metabolic disturbances - hypoglycaemia
```
75
what is the most important thing to do when you see somebody having a seizure?
start a timer + call for help + establish IV access if possible
76
management of status epilepticus in the first 0-5 minutes
secure airway - semi-prone position, nasoparyngeal airway
start regular monitoring - GCS, pulse, BP, temp, ECG
give high concentration oxygen
give high potentcy thiamine if there is any suggestion of alcohol abuse or impaired nutrition
give glucose if pt is hypoglycaemic
77
management of status epilepticus in the 5-20 minutes
if seizures continue, the ngive benzos
- if in community, buccal midazolam or rectal diazepam
- if IV access established - 4mg lorazepam stats
- if no response to 1st benzo after 10-20 minutes, give another dose
78
what are the investigations regimen for status epileptics
| in 5-20 minutes
bloods - FBC, U&E, LFT, blood gas, calcium, magnesium, CRP, clotting, glucose, anticonvulsant drug levels
establish medical history
request CXR to assess for possible aspiration
request urgent CT head if no previous history of epilepsy or new focal nuerology
79
management of status epilepticus at 20-40 minutes
> 30 minutes = satus epilepticus
alert anaesthetist and ICU & consider phenytoin. Senior decision
80
when should you call an ambulance if someone has a seizure in a GP practice
5 minutes after 1st dose of Benzo + still seizure
81
what is the most common aetiology of olfactory nerve damage/lesion
trauma - impact to the lateral and occipital regions
intracranial space - occupying lesion
82
clinical features of olfactory nerve lesion
anosmia
83
what is the most common aetiology of optic nerve damage/lesion
ischaemic optic neuropahty
trauma
optic nerve glioma
amiodarone/ethambutol
84
clinical features of olfactory nerve lesion
impaired vision
complete transection - ipsilateral blindness and loss of direct pupillary response
85
what is the most common aetiology of oculomotor damage/lesion
diabetic cranial mononeuropathy
posterior communication artery aneurysm
86
clinical of oculomotor nerve lesions
paralyic squint - adduction weakness
ptosis
the affected eye will have a down and outward appearances
horizontal diplopia - worse when head is turned away from the side of nerve palsy
87
diagnostic test for oculomotor nerve lesion
if dilated pupil
- compressive lesion eg posterior communicating aneurysm
- MRI imaging
pupillary sparing
- ischaemic microangiopathy
- assess for RF of atherosclerosis if no improvement in 3 months --> MRI
88
management of oculomotor nerve lesion
if compressive lesion - surgery
posterior communicating aneurysm - endovascular coiling and clipping
89
what is the most common aetiology of damage to trochlear nerve?
microvascular damage
Cavernous sinus thrombosis
90
clinical features of trochlear nerve damage
affected side --> eyeball drift upward and inward
diplopia
91
function of cranial nerve 5
trigeminal nerve
sensory - 3 branches for the 3 areas of the face . afferent arm of corneal reflex
motor - muscle of mastication
92
what is the most common aetiology of damage to trigeminal nerve?
inflammation of the nerve
cavernous sinus thrombosis
93
clinical features of trigeminal nerve damage
inability to feel in all 3 branches of the face eg opthalmic, maxillary and mandibular region
jaw deviates towards side of the lesion
can get trigeminal neurolgia
94
what is the most common aetiology of damage to abducens nerve?
cavernous sinus thrombosis
95
clinical featuers of abducen nerve damage
horizontal diplopia
esotropia - affected eye in-turning
96
what is the commonest facial nerve damage/lesions
trauma
Bell's palsy - viral infection leading to temporary dysfunctioning of the nerve
97
what is the commonest Vestibulocochlear nerve damage/lesions
Lyme's disease - ticks
98
clinical features of vestibulocochlear nerve damage/lesions
sensorineural hearing loss
vertigo
horizontal nystagmus
99
what is the commonest glossopharyngeal nerve damage/lesions
often unknown and rarely a mononeuronal damage
100
clinical features of glossopharyngeal nerve damage/lesions
loss of gag reflex
loss of carotid sinus reflux
sensory loss soft palate, upper phalanx, posterior 1/3 of tongue
mild dysphagia
101
what is the commonest vagus nerve damage/lesions
trauma
DM
inflammation
aortic anuerysm
102
clinical features of vagus nerve damage/lesions
gag reflex absent
deviation of uvula away from the the side of lesion
epiglottic paralysis
dysphage
vocal cord paralysis - hoarseness
103
what is the commonest accessory nerve damage/lesions
surgeries in the lateral cervical regions
104
clinical features of accessory nerve damage/lesions
paralysis of SCM and trapezius
105
what is the commonest hypoglossal nerve damage/lesions
tumours
trauma
106
clinical features of hypoglossal nerve damage
atrophy and fasciculation of the tongue
tongue deviates towards the side of lesions
107
what are some of the investigations for peripheral nerve injury
clinical examination
neurological exmaination of the area/limbs affected eg upper limb neuro exam
CT/MRI - evaluation of causes like nerve tumours, avulsions and focal soft tissue pathologies
nerve conduction studies
108
what are the 2 conditions results from brachial plexus injuries
Erbs' palsy - injury to the upper trunk of the brachial plexus (c5-c6)
Excessive lateral flexion of the neck, physio,
Waiters tip position
Rx: immobilisation in flexion/extension with and abduction brace, physio, surgery
klumpke palsy - injury to lower trunk of the brachial plexus (c8-t1)
Hyperabduction of the arm/ compression (Pancoast tumour)
Claw hand
Rx: splint, physio, surgery.
109
which nerve is damage if infraspinatus and supraspinatues muscle injury
suprascapular nerve - limited abduction and abbuction and external rotation of the arm
shoulder instability
110
which nerve is damage if latissimus dorsi and teres major muscle injury
thoracodorsal nerve - limited shoulder retarction, impaired adduction and internal rotation of the arm
111
which nerve is damage if serratus anterior muscle injury
long thoracic nerve injury - medial winging of the scapula, impaired abduction of the arm
112
which nerve is damage if rhomboid major and minor, levator scapulae muscle injury
dorsal scapular nerve injury - lateral winging of the scapula
113
which nerve is damage if gluteus medius and minimus muscle injury
superior gluteal nerve injury - paralysis of gluteus medius and minimus, Tension fascia lata --> Inter hip abduction
Positive Trendelenburg sign - lateral pelvic titlt towards the opposite side
114
which nerve is damage if Gluteus maximus muscle injury
inferior gluteal nerve - paralysis of gluteus maximus - impaired thigh extension
Standing from sitting position and climbing stairs
Backward lunching gate - Trying to use backwards during the heelstrike face in the lane with a weak hip extension
forward pelvic tilt
115
which nerve is damage if hip flexion is impaired
femoral nerve injury - paralysis of quadricep muscle and anterior medial thigh sensation
116
which nerve is damaged if pain and paresthesia on the lateral surface of the anterior thigh
lateral femoral cutaneous nerve
117
which nerve is damaged if paralysis of hip adductors
obturator nerve - usually due ot pelvic ring fracture
118
which nerve is damaged if paralysis of foot and toe extensor (dorsiflexor)
common peroneal nerve injury - paralysis of foot and toe extensor (dorsiflexors) - foot drop - high-steeping gait
impaired pronation of the foot
119
which nerve is damage if posteriolateral side of the lower leg, the lateral border of the foot and small area under the heel
sural nerve injury
