Approach to a patient presenting with limb weakness.

1. APPROACH TO A PATIENT
WITH LIMB WEAKNESS
BY
ANUJ SHAH
OCUNGKOMA SIMON
Dr. SENDIKADIWA CHARLES

2. OBJECTIVES
 Case summary
 Classification of limb weakness
 Etiology and risk factors
 Signs used to distinguish the
origin of weakness
 Pathogenesis
 Upper motor neuron weakness
 Lower motor neuron weakness
 Neuromuscular junction
weakness
 Myopathies weakness
 Psychogenic weakness
 Distribution
 Hemiparesis
 Paraparesis
 Quadriparesis
 Monoparesis
 Distal vs Proximal weakness
 Approach to a patient with
limb weakness
 History taking and
examination
 Investigation and
management

3. CASE SUMMARY
 K.E a 39y/M a known HTN who has been on medication for about a year but defaulting, referral from
Kiruddu hospital for surgical management of a blood clot in the brain, presented with a sudden loss
of consciousness following a collapse while digging and it was associated with vomiting(greenish in
color), right sided body weakness, hemiparalysis, facial drooping and severe thunderclap headache.
However, there was no fever, seizures, dizziness, blurring of vision, paresthesia or tinnitus. Patient
report having been shot in 2011 and has a bullet lodged in his right hemi-thorax, no known food or
drug allergy and no known history of any other chronic illness.
On general examination
Sick-looking, restless and afebrile (JACCOLD)◦
CNS examination: patient was awake and restless with GCS of 12/15, E.4, M.6, V.2. Reduced muscle
power on the right side.
RESP: on auscultation there was vesicular breath sounds with no added sounds. SPO2 98% on room air.
CVS: apex beat was felt at the 5th intercostal space mid-clavicular line. Heart sound S1 and S2 were
heard.
Blood pressure 220/127 mmHg
Pulse 60 b/m
Respiratory rate 22b/m
Temperature 38
Sp02 =98% on room air

4. Physical examination with respect to CNS /MSS
Findings: reduced muscle bulk in anterior –posterior compartment in all the limbs
,normal tone in all upper and lower limbs, normal muscle power in the left and right
upper limbs (5/5) and reduced muscle power on the right upper and right lower
limbs (0/5), normal findings on superficial reflexes ,on the left upper and left lower
limbs ,absent reflexes on the right limbs.
IMPRESSION
Acute hemorrhagic stroke
Hypertensive crisis
PLAN
 Investigation
LABARATORY TESTS : CBC ,MRDT/Malaria BS,LFTs ,RFTs,
IMAGING : brain CT , ECHO.

5. RESULTS
CBC :pending.
RFTS: normal Creatinine levels, elevated urea nitrogen at 19mg/dl.
LFTS ; low ALP.
Lipid profile: elevated serum triglyceride at 225mg/dl, cholesterol at 152mg/dl.
MRDT : Negative, Malaria BS –no malaria parasites seen
ECHO: hypertensive heart disease, concentric ventricular hypertrophy. Grade I
left ventricular diastolic dysfunction. tension
Brain CT : hyperdense lesion in the left parietal lobe, Basal ganglia area with
intraventricular extension. No midline shift.

6. DIAGNOSIS
 Acute hemorrhagic stroke
 Hypertensive heart disease

9. CAUSES OF LIMB WEAKNESS
 Upper motor neuron lesions
These can be due to ;-
1. Spinal lesion ( stroke, hemorrhage, mass)
2. Multiple sclerosis ( often unilateral)
3. Cerebral lesion (stroke, hemorrhage and mass)
 Spinal Cord Compression
Extradural(lesion in the vertebral column) 80%
 Trauma
 TB of spine
 Lymphoma
 Secondary deposits, in the elderly
 Multiple myeloma in elderly
 Abscess

10. Continuation…
 Intradural (extramedullary and intramedullary )
a. Extramedullary(within dura) 15%
• Meningioma
• Neurofibroma
• Secondary deposits
• Lymphoma
• Leukemia
b. Intramedullary 5%
• Glioma
• Ependymoma
• Syringomyelia
 Vascular
• Haemorrhage
• Infarction

11. Continuation…
 Systemic degeneration of tracts
• Multiple sclerosis
• Motor neuron disease (MND): Progressive muscular atrophy (predominantly LMN),
Primary lateral sclerosis (predominantly UMN), progressive bulbar
palsy(predominantly cranial nerve) and amyotrophic lateral sclerosis(mixed UMN &
LMN)
• Subacute combined degeneration of the cord (vitamin B12 deficiency)
 Infection
• Neurosyphilis
• Transverse myelitis
 Cerebral lesion (uncommon)
• Thrombosis of superior sagittal sinus
• Tumor of falx cerebri (parasagittal meningioma )
• Multiple cerebral infarction
 Hydrocephalus
• In a child-cerebral palsy (usual lesion is bilateral parasagittal cortical lesion )
• Thrombosis of unimpaired anterior cerebral artery

12. Continuation…
LOWER MOTOR NEURON LESIONS
 Anterior horn cell
 Poliomyelitis
 Motor neuron disease
 Peripheral nerves
 Peripheral neuropathy (Guillain-
Barre syndrome )
DISTINGUISING B/W UPPER AND
LOWER MOTOR NEURON

13. Continuation
 Myositides: 1. dermatomyositis
2. necrotizing myositis
3. polymyositis
 Endocrine causes: 1. Adrenal insufficiency(Addison disease) (generalized)
2. hyperthyroidism
3. cushing syndrome
4. hypothyroidism
5. secondary hyperparathyroidism
6. diabetes mellitus
 Genetic: 1. becker muscular dystrophy
2. glycogen and lipid storage diseases, mitochondrial diseases
3. limb-girdle muscular dystrophy
4. mytonic dystrophy type 1
 Medications: 1. fluoroquinolones (tendon swelling or rupture) (distal)
2. glucocorticoids
 Toxins: alcohol

14. PARAPLEGIA OF
SUDDEN ONSET
 Trauma (to vertebral column)
 Collapse of vertebra due to any
cause
 Multiple sclerosis
 Anterior spinal artery occlusion
 Dissecting aneurysm
 Post infectious or post-vaccinal
myelitis( Transverse myelitis

15. LIMB WEAKNESS ACCORDING TO ONSET

16. DIFFERENTIAL DIAGNOSES ACCORDING
TO ONSET OF LIMB WEAKNESS
 Fulminating (seconds to minutes)
 Drop attacks
 Haemorrhage (epidural or intraspinal) Acute (hours to several days)
 Inflammatory transverse myelitis (post-infection, post-vaccination)
 Demyelinating transverse myelitis (multiple sclerosis)
 Compressive myelopathy
 Polyneuropathies (Guillain–Barré syndrome, tick paralysis, botulism,
diphtheria)
 Spinal cord stroke (rarely brainstem or bilateral cortical stroke)

17. Cont….
 Familial periodic paralysis (usually hypokalaemic, rarely hyperkalaemic)
 Metabolic myopathy (hypercalcaemia, hypokalaemia, drug induced)
 Hysterical conversion disorder Subacute (days to several weeks)
 Compressive myelopathy
 Intrinsic spinal cord lesion
 Meningeal carcinomatosis (multiple nerve roots)
 Myopathies (inflammatory, metabolic – hypercalcaemia, hypokalaemia,
hypothyroid, hyperthyroid, and drug induced)
 Chronic inflammatory demyelinating polyneuropathy
 Neuromuscular junction diseases (myasthenia gravis, myasthenic syndrome)

18. DISCUSSION
Normal motor function : Cerebral cortex ,Basal ganglia ,cerebellum ,red nucleus
,brain stem reticular formation ,lateral vestibular nucleus and spinal cord
 Motor system dysfunction
 Weakness or paralysis
 Ataxia
 Abnormal movements
 Weakness reduction in power
o Prefix and suffix
• -Plegia
• -Paresis
• Hemi-
• Para-
• Quadri-

19. ORIGIN OF WEAKNESS
signs to distinguish the origin of weaknesss
SIGN UPPER MOTOR NEURON LOWER MOTOR
NEURON
MYOPATHIC PSYCHOGENIC
Atrophy None Severe mild none
fasciculation none common none none
tone spastic decreased Normal
/decreased
Variable
/paratonia
Distribution of
weakness
Pyramidal/regional Distal/segmental Proximal Variable/inconsist
ent with daily
Muscle stretch
reflexes
Hyperactive Hypo-active
/absent
Normal/hyp
oactive
normal
Babinski Present Absent Absent normal

20. Cont..
 Muscle bulk
• UMN Normal or mild disuse atrophy
• LMN severe atrophy
• Advanced myopathy atrophy (less severe than LMN
 Distribution of weakness
UMN Extensors and abductor of UL ,Flexor of LL
LMN level of involvement ;AHC /nerve root /limb plexus or peripheral nerve
Myopathic weakness of proximal muscles
Impaired NM junction transmission no specific pattern fatigability
Tone Resistance to passive stretch
 Increased
Spasticity UMN ,velocity dependent (clasp knife , antigravity muscles )
Rigidity extrapyramidal lesions present throughout motion (led pipe ,flexor =extensors
Paratonia (Gegenhalten ;frontal lobe ,variable tone throughout motion
 Decreased (flaccidity
LMN palsy

21. Cont..
 Muscle stretch reflexes
UMN increased : may be decreased /absent for a variable period ,extensor
plantar response (Babinski ,loss of cutaneous reflexes
LMN decreased
Myopathic preserved ,late stages =attenuated
NM junction disorders
 Myasthenia gravis
 Lambert Eaton syndrome
Fasciculation

22. Clinical pathway to diagnosing sudden limb
weakness.

23. PATHOGENESIS
 UMN
Decreased activation of lower motor neurons
Distal muscle groups >proximal muscles
Axial sparing
Spasticity
Corticobulbar ;lower face ,tongue
B/L Corticobulbar :Psuedobulbar palsy
 UMN
Disorder of LMN in brainstem motor nuclei ,anterior horn cells in spinal cord or axonal
dysfunction of these neurons
Loss of alpha motor neurons >decreased activation of muscles fibers
Loss of Gama motor neurons
Fasciculation ;when a motor unit or alpha motor neuron unit degenerate

24. PATHOGENESIS
 NM junction weakness
Weakness of variable degree and distribution
Depends on state of rest of NM junctions
Preceding activity influences strength
Fatiguability
 Myopathic weakness
Decreased in number or contractile force of muscle fibers activated with in
motor units
Muscular dystrophies ,inflammatory myopathies or myopathies
EMG ;size of each motor unit action potential is increased
 Psychogenic weakness
Without any organic basis
Variable ,inconsistent , unexplainable pattern of distribution
How to rest?

25. Pattern of weakness
 MONOPLEGIA – weakness of a limb
 Lesion often cortical, vascular in etiology
 Sometimes, peripheral n lesion

 HEMIPLEGIA – weakness of upper & lower limbs on same side
 Usually UMN
 Lesion at cortex, internal capsule
 Sometimes, brain stem/SC lesions
Signs:
 hand preference before 2 yrs. of age
 circumduction gait
 asymmetrical reflexes
 hemiplegic hand kept flexed at elbow, fisted with adducted thumb
Causes:
 Hemiplegic cerebral palsy
 Todd's palsy
 Tumor
 Trauma

26. Cont…
PARAPLEGIA: Weakness of both lower limbs
 Lesion in SC or PN (polyneuritis)
 UMN type – lesion in SC. If acute may  spinal shock
 LMN type -
- lesion in lower SC e.g. myelomeningocele
- spinal shock stage
- polyneuritis eg GBS, post diphtheritic palsy
- NM junction
- Muscle

27. Cont…
SPINAL CORD LESIONS:
 I Compressive
 Acute – trauma, epidural abscess
 Chronic –tumor, vertebral disease, syringomyelia, arachnoiditis

 II Non compressive
 Acute – TM, hematomyelia, infarction, infections, post infectious
 Chronic – degenerative
 -spinocerebellar degenerations
 -spinal muscular atrophy
 -motor neuron disease
 -subacute combined degeneration
Chronic lesions may present acutely dt secondary vascular changes

28. Continuation…
QUADRIPLEGIA- weakness of all 4 limbs
· Deep coma
· Lesions of brain stem
Upper SC  UMN signs
· Polyneuritis
All causes of paraplegia
Craniovertebral malformations
DIPLEGIA- weakness of both arms or both legs
 Cerebral diplegia – a form of CP seen in premature babies

30. DISTRIBUTION
DISTAL WEAKNESS PROXIMAL WEAKENESS
Two or more limbs distally –LMN or
peripheral nerve
Myopathy
Acute toxic polyneuropathy NM junction weakness
Cauda Equina syndrome AHC disease
Distal symmetric weakness –Associated
with numbness –Peripheral neuropathy
No numbness
AHC disease may begin distally –
Asymmetric ,No numbness
Evaluation CK ,Electrophysiologic
studies

31. APPROACH TO A PATIENT WITH LIMB WEAKNESS
HISTORY TAKING AND EXAMINATION
History taking
Bio data Name, Age ,Sex ,Occupation, Tribe, Religion ,Education, Marital status, address, DOA, referral
Presenting Complaint
&
History of Presenting
complaint
Reason for coming to the Health Facility and reason for referral
The interviewer asks open ended questions to determine the nature ,duration of symptoms and
any other associated factors
Take complete history of the presenting complaint which involves duration of symptoms
associated symptoms of presenting complaint, relieving or exacerbating factors
Past medical and past
surgical history
The interviewer asks admission for chronic illness , history of allergies to food or drugs .
He also asks history of a major trauma to head or spine ,history of major surgical procedures and
blood transfusion
Background Family history
Social history

32. EXAMINATION
General examination relevant to CNS and Musculo-skeletal system
Physical examination : CNS /MSS
Inspect for symmetry ,fasciculation ,visible masses and any other abnormalities
B-Muscle bulk
T-muscle tone
P- Muscle power
R-reflexes
 Superficial reflexes
 Deep tendon reflexes

33. INVESTIGATION
 X-ray of the lumbo-dorsal spine (AP and lateral )
 CT or MRI
 CSF study
 Other tests according to cause (TB ,Myeloma)
 Nerve conduction studies
 Electromyography (EMG)

34. MANAGEMENT
 SPECIFIC MANAGEMENT
In our presented case:
Seizure prophylaxis : I.V phenytoin 250mg bd for three days
BP management : labetolol 40mg every 20mins (3 doses)
Pain management : IV paracetamol 1g tds for 3 days
Antipsychotics : IM haloperidol 10mg OD for 3 days
Osmotic diuretic : hypertonic solution 3% in 100mls 8 hoursly for 2 days
In other cases
Pott’s disease : Anti-tubercular therapy ,surgery
Ataxia telangiectasia mutated : Initially I.V glucocorticoid ,then oral prednisolone
Guillain-Barre Syndrome ;IV Ig (400mg /kg/day )for 5 days
Subacute combined degeneration of the spinal ; Injection Vitamin B12 1000 micro gm
IM- 5 doses then every 3 months for lifelong
Multiple sclerosis ; IV methylprednisolone or interferon B
Spinal cord tumor :surgery

35. References
 Davidson’s Principles and Practice of Medicine 23rd Edition
 Harrisons Principles of internal medicine 20th Edition
 Oxford handbook of Clinical Medicine 9th Edition
 Muscle Weakness in Adults: Evaluation and Differential Diagnosis Scott T.
Larson, MD, and Jason Wilbur, MD, University of Iowa Carver College of
Medicine, Iowa City, Iowa