Revisin Flashcards
what are 2 possible side effects of a statin
muscle pain and weakness
what do you worry about with night pain
cancer
what are spinal red flags
back pain (worse at night, new pain in old patient)
bilateral sciatica, urinary incontinence
impotence
saddle anaesthesia
what is cauda equina syndrome
Compression/ irritation of lumbosacral nerve roots below conus medullaris
what are the common causes of cauda equina syndrome
herniated disc, spinal stenosis, vertebral fracture, tumour
what are the clinical features of cauda equina syndrome
usually acute (<24hrs), rarely subacute or chronic. Motor signs - LMN signs → weakness in multiple root distribution, reduced tendon reflexes Sensory signs - low back pain radiating to legs aggravated by sitting, relieved by lying down. Saddle anaesthesia (S2-5) Autonomic signs - urinary retention/ overflow incontinence, loss of anal tone (faecal incontinence).
treatment for cauda equina
PR
MRI of lumbar spine
decompression within 48 hrs
what reflexes are usually absent in cauda equina
ankle
where does the conus medullaris end
L1/2
what is degenerative cervical myelopathy
spinal cord dysfunction from compression in the neck.1 Patients report neurological symptoms such as pain and numbness in limbs, poor coordination, imbalance, and bladder problems. Owing to its mobility, the vertebral column of the neck is particularly prone to degenerative changes such as disc herniation, ligament hypertrophy or ossification, and osteophyte formation
what are the common symptoms of degernative cervical myelopathy
Neck pain/stiffness
Unilateral or bilateral limb/body pain
Upper limb weakness, numbness, or loss of dexterity
Lower limb stiffness, weakness, or sensory loss
Paraesthesia (tingling or pins and needles sensations)
Autonomic symptoms such as bowel or bladder incontinence, erectile dysfunction, or difficulty passing urine
Imbalance/unsteadiness
Falls
what are the motor signs of degenerative cervical myelopathy
o Pyramidal weakness (Upper limb; extensors more than flexors. Lower limb: flexors more than extensors)
o Limb hyperreflexia
o Spasticity (eg, clasp knife sign)
o Clonus, especially Achilles tendon
o Hoffman’s sign (thumb adduction/flexion +/− finger flexion after forced flexion and sudden release of a finger, distally)
o Babinski’s sign (upgoing plantar)
o Segmental weakness (corresponding to the level of compression)
what are the features of an upper motor neurone lesion
paralyses affects movement rather than muscles slight muscle wasting spasticity hyperreflexia hypertonia normal power
what are the features of a lower motor neurone lesion
flaccid paralysis (of muscle or muscle group) severe atrophy hypotonia absent reflexes may have fasciculation and fibrillation
what is the most likely benign tumour of the brain
meningioma
what is foster kennedy syndrome
when a slow growing frontal lobe tumour compresses optic nerve causing it to atrophy
what level in spinal cord do sensory afferent from bladder enter
S2-4
what is danish
how to examine to cerebellum
- dyskensia
- ataxia
- nystagmus
- intention tremor
- staccato speech
- hypotonia
what tract will an upper motor neurone be in
pyramidal tracts
is parkinsons an UMN lesion
no as not within the pyramidal tract
are tremors pyramidal or extrapyramidal
extra pyramidal (involuntary movements)
where are LMNs
anywhere below L1/2 or out with the CNS
what is a tremor
involuntary movement in which there is rhythmicity, is a regular movement
what movements tend to develop in extrapyramidal disorders
involuntary- tremors
what are the types of tremors
resting- when sitting and relaxed
postural- holding arms in certain postitions
intention- when trying to complete an action
where must a lesion be if it affects the leg and arm
cervical spin or above
weakness is a symptoms of a lesion affecting which tract
pyramidal
why is there not weakness in parkinsons
as extrapyramidal
what are the hallmarks of parkinsons
SLOWNESS (bradykinesia- only symptoms seen in everyone)
tremor
tone (stiffness and rigidity)
what are the other symptoms of parkinsons
can 'freeze' and struggle to initiate and stop movements shuffling gate stooped posture changes in mood handwriting gets smaller (micrographia) balance problems depression and anxiety sleeping problems loose paralysis in dreams so cant act out what they are dreaming REM sleep disorder loose sense of smell and taste (before motor symptoms) memory changes voice gets quieter constipation bladder problems
where is the lesion in parkinsons
substantia nigra in the basal ganglia (produces dopamine)
why is cerebrovascular pmhx important in parkinsons
as type of vascular parkinsons
what diseases are related to parkinsons
cerebrovascular disease, psychiatric problems (anti dopamine drugs)
what drugs are related to parkinsons
antihistamines, anti emetics (block dopamine), some anti psychotics
what are the risk factor for parkinsons
family Hx
risk factors for cardiovascular disease- alcohol, diet etc
NOT SMOKING - smoking protects you from parkinsons
what occupations have increased risk of parkinsons
agriculture, manganese minors, general exposure to chemicals
what is the commonest form of parkinsons
idiopathic
what type of movement do you loose in parkinsons
spontaneous
- facial
- adjusting position
- rolling over in bed
are cranial nerves affected in parkinsons
no
how is tone affected in parkinsons
increased (not in same way as UMN lesion)
= rigidity (high tone but velocity independant)
also get cog wheel rigidity
what type of tone changes in UMN lesion
velocity dependent
spactity
hypertonic
what type of tone changes in LMN lesion
hypotonia
flaccidity
does parkinsons affect one or both sides
affects both sides of the brain but to different degrees so usually have one side affected in early stages then becomes more symmetrical
how is power affected in parkinsons
isnt as extrapyramidal
are reflexes affected in parkinsons
no as reflexes are pyramidal
is coordination affected in parkinsons
no as cerebellum fine
what do yuo get a resting tremor in
parkinsons
what do you get a postural tremor in
drugs, dystolic tremor, anxiety
what do you get an intention tremor in
cerebellar disease
what is a holmes tremor
a resting, postural and intentional tremor all at the same time
what is bradykinesia
slowness with decrement and degradation of repetitive movements (“fatigue”)
what are is affected in a central nervous system lesion
hemiplegia/ paraplegia/ whole limb
what type of weakness in a central nervous system lesion
heaviness
what are the additional features of a central nervous system lesion
spasms/ jerks
cognitive/ sphincter involvement
can you get sensory symptoms in a central nervous system lesion
yes
what area will be affected in a peripheral nervous system lesion
may be peripheral or localised areas
can be whole limb if affects plexus
what type of weakness in a peripheral nervous system lesion
positional/ with sleep
ascending
what additional features can exists in a peripheral nervous system lesion
cramp twitching (fasciculations) loss of grip tripping up unsteady with eyes closed
can you get sensory symptoms in a peripheral nervous system lesion
yes
pain may be prominent
where might be affected in NMJ lesion
ocular/ bulbar/ proximal limb
what is the weakness like in a NMJ lesion
fatiguable - worse after use
diurnal variations- worse towards end of day
what additional features can be seen in a NMJ lesion
bulbar- swallowing, speaking, loss of chewing/ talking
ocular- diplopia, ptosis, prolonged gaze hard
resp- orthopnoea
can you get sensory symption in a NMJ lesion
no
where might be affected in muscular lesion
proximal
symmetrical
what is the weakness like in a muscle lesion
may be aching
may be insidious
proximal weakness
symmetrical
what additional features can you get in a muscle lesion
myalgia
cramping
hard to get up from low chairs/ hang out washing
can you get sensory symptoms in a muscle lesion
no
what might be seen on inspection in a CNS lesion
abnormal limb posture
what might be seen on inspection in a PNS lesion
wasting/ fasciculations
pes cavus
what might be seen on inspection in a NMJ lesion
ptosis
ophthalmoplegia
what might be seen on inspection in a muscle lesion
proximal wasting
what happens to tone in a CNS lesion
increased
spacticity/ clonus
what happens to tone in a PNS lesion
decreased
what happens to tone in a NMJ lesion
normal or decreased
what happens to tone in a muscle lesion
normal or decreased
what is the pattern of weakness like in peripheral neuropathy
distal weakness
what is a pyramidal pattern of weakness
arm: extensors weaker than flexors
leg: flexors weaker than extensors
if brain affected= contralaterla
if cord affected= ipsilateral side
what are reflexes like in a CNS lesion
increased
what are reflexes like in a PNS lesion
decreased
what are reflexes like in a NMJ lesion
normal or decreased
what are reflexes like in a muscle lesion
normal or decreased
what are reflexes like in a CNS lesion
extensor
what are reflexes like in a PNS lesion
flexor/ mute
what are reflexes like in a NMJ lesion
flexor
what are reflexes like in a muscle lesion
flexor
what distribution of sensory symptoms in a CNS lesion
brain- hemi sensory (one side for body, other side for face (trigeminal nerve))
cord- at sensory level
what distribution of sensory symptoms the PNS lesion: sensory neuropathy
glove and stocking
what distribution of sensory symptoms the PNS lesion: root/ plexus/ mononeuropathy lesion
depends on dermatome/ nerve
what does velocity dependant increased tone mean
involves pyramidal tract
where will see the effects of a lesion in the internal capsule
leg, arm, face and trunk
what is the general pattern of an inflammatory lesion in the brain
relapsing and remitting
what are the types of NMJ pathology and how can you differentiate them
lambert eaton= diminshed/ adbscence deep tendon reflex, autonomic features (is a pre synaptic problem)
myaestenia gravis - has ocular problems (post synaptic problem)
how do you demonstrate NMJ pathologies
bulbar- counting out loud ocular- fixed horizontal gaze ptosis- fixed upward gaze limb- repetitive movements (fatiguing weakness)
what results from an L4/5 L5 impingement
weak toe dorsiflexion
what results from an L5/S1 S1 impingement
weak knee flexion
decreased knee jerk
what happens in a lesion on the brachial plexus
extensive arm weakness
what happens in a lesion on the lumbosacral plexus
extensive leg weakness
what results from a median nerve neuropathy
weak thumb abduction
what results from a ulnar nerve neuropathy
weak finger abduction
what are 2 features and common causes of peripheral neuropathy
is distal and sensory more than weakness
if acute- guillane barre syndrome
if chronic- diabetes/ alcohol
what test do you always do in epilepsy
ECG!!!!!
what does rigidity occur in
extrapyramidal conditions affecting the basal ganglia (e.g. parkinsons)
is rigidity associated with weakness
no
but can have slow developing muscle contractions (bradykinesia)
is there usually a change in tendon reflexes in rigidity
no
what is spasticity dependent on
(velocity)
input to the spinal cord produced by the passive movement of the limb
which muscles is spasticity predominantly found in
flexor muscles and forearm pronators inarm
extensor muscles in the legs
(think opposite to pyramidal weakness)
what is the clasp knife phenomonenum
where spasticity builds up soon after the start of the passive movement, then melts away
how is spasticity most easily elicited in the arm and leg
rapid extension of the elbow or supination of
the forearm
in the leg by rapid flexion of the knee
will a slow movement meet resistance in spasticity
no
what are the features of rigidity that distinguish it from spasticity
not velocity dependent
present equally in flexors and extensors
present throughout the range of movement
can have cog wheel or led pipe quality
how is rigidity best elicited
relatively slow passive movements
In the arm by flexion-extension of the wrist and elbow, and by supination-pronation of
the elbow.
In the lower limb flexion-extension of the knee and ankle are tested
what is the MRC power scale
0= No contraction
1= Flicker of contraction without movement
2= Slight movement with gravity eliminated*
3= Movement against gravity only
4= Movement against resistance
(can expand grade 4 to: 4+, 4 and 4-)
5= Normal power
why do tendon reflexes change
Reflexes are very sensitive to pathology affecting the afferent side of the reflex arc. If
conduction is blocked in only a few muscle spindle primary afferents, then the
compound action potential elicited in all the motorneurones will be smaller, and the
reflex will be less brisk or absent.
Reflexes are also sensitive to “upper motorneurone lesions” affecting the descending
motor pathways in the cerebral hemispheres, brainstem and spinal cord. The
excitability of the alpha motorneurones increases and the reflexes become brisker.
when is clonus abnormal
when it is sustained
what is reinforcement when testing a reflex
e.g.to link the fingers of each
hand and attempt to pull them apart to test lower limb reflexes
what is clonus
the rhythmic contraction of a muscle group elicited by a rapid passive stretch of it
what is the triceps surae
pair of muscles located at the calf - the two-headed
gastrocnemius and the soleus- ankle extensors- common to get clonus here
what is clonus a sign of
UMN lesions
always associated with brisk ankle jerks
when are reflexes abnormal
when they are absent (with reinforcement).
when they are asymmetrical (right v left).
when there is a marked discrepancy between different reflexes (eg between those
in the arms and those in the legs).
when there is sustained clonus.
what is a positive babinski response
big toe extends and the other toes fan- sign of UMN lesion
what is a spastic gait
due to UMN lesion
affected limbs appear very stiff
what causes a parkinonian gait
basal ganglia pathology
what causes a truncal ataxia (widebase, unsteady)
cerebellar disease
hydrocephalus
proprioceptive loss (neuropathy/ myelopathy)
what causes a high stepping gate
biltaeral= peripheral neuropathy unilateral= peroneal nerve or L4 root lesion
what causes a waddling gait
proximal leg weakness
what are the types of tremor
Rest: Present when the subject is relaxed, and decreasing on
maintaining a posture or during movement
Postural/Action: Present on maintaining a posture and during movement, but
disappearing at rest.
Intention: Present towards the end of a movement to a target, causing
overshoot (dysmetria).
what are the causes for resting tremor
parkinsons
what are the causes for postural/ action tremor
Physiological
Essential tremor, drugs
Anxiety, Thyrotoxicosis
what are the causes for intention tremor
cerebellar disease
what happens to rapid supination/ pronation movements in parkinsons
In extrapyramidal diseases (Parkinsonian syndromes) there is a reduction in
the amplitude and speed of supination/pronation movements.
what happens to rapid supination/ pronation movements in cerebellar disease
irregularity of the movements as well as slowing
and reduction in amplitude.
how do different pathologies affect fine finger movement
impaired in upper motor neurone lesions affecting the hand,
particularly with cortical lesions when the hand may be clumsy with little
weakness.
Fine finger movements are also impaired in extrapyramidal
diseases and cervical myelopathy.
what type of taste do the CN VII an IX nerves carry
sourness
sweetness
bitterness
saltiness
what vision loss in optic neuritis
central scrotoma
what causes red vision to be lost
optic nerve dysfunction
where is a defect if vision loss is homonymous
behind the chiasm
what is a hippus
oscillation in pupillary size
what is the pupil like in horners syndrome
miotic (constricted)
will also have lack of upward gaze
what is bells phenomenon
the upward deviation of the eyes on closure
what causes diplopia when only one eye is open
refractive error or cerebellar problem
what causes vertical upbeat nystagmus
most commonly seen as a side-effect of anticonvulsants but it may also occur in cerebellar and pontomedullary abnormalities and in Wernicke’s encephalopathy
what causes down beat vertical nysatgmus (fast downward phase)
abnormality at the craniocervical junction
cerebellar degeneration and drug intoxication
Wernicke’s encephalopathy, demyelination, brain stem encephalitis, tumours at the foramen magnum and hydrocephalus.
is there diplopia in long standing strabismus
no
what does the medial longitudinal fasciculus connect
CN III, IV and VI
in the trigeminal nerve, what are the central connection for touch and pain/ temperature afferents
touch = main sensory nucleus
pain/ temp= spinal nucleus
where does UMN facial weakness tend to spare
the upper half of the face
what nerve supplies taste to the anterior 2/3rds of the tongue
CN VII (facial)
what does a corrective saccade in the head thrust test mean
a peripheral cause of vestobular problems
does the spinal accessory nerve originate from cord or brain stem
both hehe
what s a bulbar palsy
(bulbar= medulla)
caused by diseases affecting the lower cranial nerves e.g. a LMN lesion, NMJ or muscle problem
what causes a pseudobulbar palsy
when a UMN lesion affects the lower cranial nerves (a disease of the corticobulbar tracts)
what can a bulbar palsy with a LMN lesion cause
-impaired voluntary palatal movement
impaired palatal movement on eliciting the gag reflex or loss of the gag reflex
wasting and fasciculation of the tongue
slurring dysarthria and dysphagia
what does a pseudobulbar palsy cause
a brisk jaw jerk a brisk gag reflex a spastic tongue (with difficulty protruding the tongue and impaired rapid tongue movements) a spastic dysarthria and dysphagia
how do you test each occular muscle and nerve (movements)
III -superior rectus (looks laterally and upwards), inferior rectus (looks laterally and
downwards), medial rectus (looks medially), inferior oblique (looks medially and
upwards)
IV -superior oblique (looks medially and downwards)
VI - lateral rectus (looks laterally)
what are the different types of articulation
Palatal articulation – “KA”,
Guttural articulation – “GO”,
Labial articulation – “PA”
what level does should abduction test
C5
what level does elbow flexion and wrist extension test
C6
what level does elbow extension and wrist flexion test
C7
what level does thumb extension test
C8
what level does finger abduction test
T1
what level does hip flexion test
L1,2
what level does knee extension test
L3
what level does ankle dorsiflexion test
L4
what level does great toe extension
L5
what level does ankle plantar flexion test
S1
what is a glioblastoma
a high grade (grade 4) astrocytoma
what is coning
where the brainstem and cerebellum get pushed through the foramen magnum (tonsillar herniation
what is cushings triad
reduced respiratory, high BP and bradycardia
happens in coning
what can cause too much CSF to be produced
choroid plexus malignancies
who gets medulloblastomas
children
what is seen pathologically in an acute infarct
oedema
discolouration (grey/ brown)
loss of normal architecture
what happens to old strokes
gliosis, liqudification by macrophages
what o watershed infarctions look like
wedge shape infarct on the peripheries of the brain
what does global hypoxia look like pathologically
mottling
loss of differentiation between grey and white matter
what are the RF for a subarachnoid haemorrhage
ADPKD
HPTx
obesity
smoking
what increases and decreases in atrophy
increase sulcus (depression- think in a sulc) decreased gyrus (bumps- think gyrating, bump and grind)
what does MS look like pathologically
dark grey spots mainly affecting white matter, periventricular
what is the lateral horn of the spinal cord
a triangular projection between the dorsal and ventral horns
it is present only in the thoracic and upper lumbar segment of the spinal cord
contains autonomic neurones (sympathetic system T1-L2)
what is the path of the dorsal column medial leminiscus pathway
primary sensory fibres travel via the posterior root ganglion
up spinal cord
synapse with 2ndary order in medulla (nucleus cuneatus if above T6, nucleus gracilis if below T6)
fibres decussate to the contralateral medial leminiscus and travel upwards to synapse in the thalamus
relayed to the ipsilateral somatosensory cortex
what is the path of the spinothalamic tract
The primary sensory axons enters the spinal cord, via the posterior root ganglion, then travel upwards for one or two segments at the periphery of the spinal cord through the tract of Lissauer to synapse in the dorsal horn.
They then cross to the contralateral side of the spinal cord to ascend to synapse in the thalamus.
Sensory signal are then relayed from the thalamus to the ipsilateral somatosensory cortex.
what is the function of the spinocerebellar pathways
provides unconscious proprioceptive information to the cerebellum, in order to coordinate posture and the movement of the lower limb and upper limb musculature.
what are the three spinocerebellar pathways and their functions
Dorsal/posterior spinocerebellar: carries unconscious proprioceptive information (from muscle spindles mainly) from the lower limbs, synapses in the dorsal nucleus of Clarke.
Cuneocerebellar: carries unconscious proprioceptive information from the upper limbs.
Ventral/anterior spinocerebellar: carries unconscious proprioceptive information (golgi tendon organs mainly) from the lower limbs then decussate twice to reach the ipsilateral cerebellum.
do the spinocerebellar tracts travel to the contra or ipsilateral cerebellum
ipsilateral
what is the role of the corticospinal tract
voluntary movements
where do the anterior corticospinal tracts decussate
the anterior white commissure
what does the anterior corticospinal tract mainly supply
proximal and axial muscles
