weakness

Question 1

UMN

Answer 1

extensors and abductors of UL. flexors of LL
spasticity, rapid repetitive movements - slow and coarse normal rhythmicity maintained.
dec activation of LMNin distance m groups accepted severely.
Corticobulbar involvement - weakness lower face, and tongue.
b/l corticobulbar lesions - pseudo bulbar palsy - dysarthria, dysphagia, dysphonia, emotional liability + b/l facial weakness, brisk jaw jerk
EMG - dec maximal discharge frequency

Question 2

LMN

Answer 2

weakness depends on the level of involvement. ant horn cells, nerve root, limb plexus. peripheral n muscle supplied by affected structure is weakened.
brain stem motor nuclei and anterior horn of spinal cord or dysfunction of axons of these neuron’s as they pass to skeletal m
weakness is due to dec in no. of muscle fibres, loss of alpha motor neurone.
loss of game motor neurone does not cause weakness

dec tension of muscle spindles, dec. muscle tone, attenuation of stretch reflex.
absent stretch is due to involvement of spindle afferent fibres.

Question 3

myopathic weakness

Answer 3

marked in proximal muscles from impaired neuromuscular transmission. no specific pattern of involvement.

Question 4

tone

Answer 4

resistance to a passive stretch. spasticity - UMN clasp knife phenomenon. affect antigravity muscles (UL flexors. LL extensors)

Question 5

rigidity

Answer 5

hypertonia through out range of movement.
lead pipe / plastic stiffness affects flexors and extensors equally

Question 6

hemiparesis

Answer 6

UMN lesion above mid cervical spinal cord, most lesions are above foramen magnum.
language d/o > cortical lesion
homonymous visual field defects > cortical/subcortical hemispheric lesion
motor hemiparesis of face, arm, leg > small discrete lesion in posterior limb of internal capsule, cerebral peduncle, upper pons
ipsilateral CN signs and contralateral hemiparesis > brain stem lesion - cross paralysis
absent CN signs of facial weakness, hemiparesis > high cervical spinal cord lesion - Brown squared syndrome

Question 7

acute or subacute hemiparesis

Answer 7

focal structural lesions, rapidly expanding lesions, or inflammatory process

Question 8

subacute hemiparesis

Answer 8

evolves over days or weeks
subdural haematoma, infectious, inflammatory d/o (cerebral abscess, fungal granuloma or meningitis, parasitic infection, multiple sclerosis, sarcoidosis) or primary and metastatic neoplasms. AIDS - due to toxoplasmosis or primary CNS lymphoma

Question 9

chronic hemiparesis

Answer 9

evolves over months
neoplasm, vascular malformation, chronic subdural haematoma, degenerative disease

Question 10

acute paraparesis

Answer 10

intra spinal lesion
sensory loss in leg, upper level on trunk, dissociated sensory loss > central cord syndrome
hyper reflexia in LL, normal reflex in arms.
imaging may reveal > compressive lesion, infarction (proprioception spared), arteriovenous fibulas, vascular anomalies, transverse myelitis.
disease of cerebral hemispheres that produce acute paraparesis > anterior cerebral artery schema (shoulder shrug affected), superior sagittal sinus, cortical venous thrombosis and acute hydrocephalus.
paraparesis after caudal equine - rare - trauma to lower back, midline disc herniation, intraspinal tutor, sphincters often affected, hip flexion spared, sensation over anterolateral thigh spared.
rare - rapidly evolving anterior horn cell disease (poliovirus, West Nile virus infection), peripheral neuropathy (GBS), myopathy

Question 11

subacute or chronic spastic paraparesis

Answer 11

UNM disease
associated with LL sensory loss and sphincter involvement, > chronic spinal cord disorder should be considered.
hemispheric signs present, parasagittal meningioma, chronic hydrocephalus likely.
absence of spasticity in a long standing paraparesis > LMN or myopathic ethology.

Question 12

investigations

Answer 12

spinal MRI,
when UMN signs with drowsiness, confusion, seizures, other hemispheric signs, brain MRI
elector physiologic studies > neuromuscular d/o

Question 13

quadriparesis

Answer 13

UMN cause suspected.
generalised weakness > disease of the motor unit is likely.
weakness form CNS disorder accompanies > spasticity, hyperreflexia, sensory disturbance.
most neuromuscular causes of generalised weakness associated with > normal mental function, hypotonia, hypoactive muscle stretch reflexes.

Question 14

causes of episodic generalised weakness

Answer 14

electrolyte abnormalities: hypo/hyper K, hyper calcemia, hypo/hyper Na, hypo phosphatemia, hypermagnesemia,
muscle d/o - channelopathies, periodic paralysis
neuromuscular junction d/o - MG, Lambert eaton myasthenic syndrome
CNS disorders, TIA, transient global cerebral ischemia, MS
lack of voluntary effort- anxiety, pain or discomfort, somatisation d/o

Question 15

acute quadriparesis

Answer 15

onset: minutes > UMN (from anoxia, hypotension, brain stem or cervical cord schema, trauma, systemic metabolic abnormalities) muscle (electrolyte disturbances, certain inborn errors of muscle energy metabolism, toxins, periodic paralysis)
onset : hours - weeks >LMN d/o GBS

investigations:
obtunded - CTB
UMN signs, alert, MRI spinal cord
LMN signs myopathic, uncertain - bloods, ck, electrolytes, EMG, NCV

Question 16

subacute/chronic

Answer 16

UMN may take weeks to years to develop > from chronic myelopathies, MS, brain or spinal tumours, chronic SDH, metabolic, toxic, infectious d/o
may result from LMN disease, chronic neuropathy, (weakness distal) myopathic weakness 9proximal weakness)

Question 17

monoparesis

Answer 17

LMN disease with or without sensory involvement.
UMN occasional - distal and non gravity muscles.
myopathic weakness rarely in one limb.

Question 18

acute monoparesis

Answer 18

distal - UMN - no sensory impairment, no pain, > likely focal schema.
sensory loss and pain accompany LMN weakness - usually localise to single nerve root or peripheral nerve, occasional plexus involvement.

LMN likely - EMG and nerve conduction study

Question 19

sub acute/ chronic monoparesis

Answer 19

weakness / atrophy - weeks to months > LMN\associated with sensory symptoms, peripheral cause (nerve, root, plexus) likely > otherwise consider - anterior horn cell disease

if weakness UMN type > discrete cortical (pre central gyrus) or cord lesion should be considered.

Question 20

distal weakness

Answer 20

> 2 limbs distally, - LMN pr peripheral nerve disease.
acute distal weakness - acute toxic polyneuropathy / caudal equine syndrome.
distal symmetric weakness - weeks to months or years associated with numbers > peripheral neuropathy.
anterior horn cell disease beings distally, asymmetric, no numbness.

Question 21

proximal weakness

Answer 21

myopathy - symmetric weakness or pelvic and shoulder gurgled muscles.
disease of neuromuscular junction (MG) - symmetric proximal muscle weakness with ptosis, diplopia, bulbar weakness, fluctuating in severity during the day.
Anterior horn cell disease - proximal weakness is asymmetric, if symmetric maybe familial. no numbness

Ix: CK, electrophysiologic studies

Question 22

weakness in restricted distribution

Answer 22

unilateral - restricted wrens due to LMN or peripheral nerve disease - facial palsy.
weakness of part of limb is commonly due to peripheral n lesions - entrapment.
symmetric, bulbar, or extra ocular muscles > myopathy, Neuro muscular junction d/o
bilateral facial palsy, areflexia > GBS
asymmetric bulbar weakness > motor neuron disease,
limited to respiratory muscles - MND, MG, polymyositis/ dermatomyositis