Approach to weakness by Internal Medicine.

1. APPROACH TO
WEAKNESS
By:-
Dr Abdul Ghani
Rahimoon
1

2. 2
Introduction:
• Weakness as professional/ medical term refer to symptom arise
from something wrong in muscle.
• In this situation very important to differentiate between
weakness & other confusing symptoms which mimic
weakness as said by patient, as fatigue.
• Weakness as mentioned before indicate the wrong is in the
muscle, either due to pathology with in muscle (myopathy), or
pathology in its motor nervous supply. So power of muscle will
be decreased according to MRC power rating system. This we
name it, objective muscle weakness, neuromuscular
weakness, true muscle weakness or clinical muscle
weakness (i.e: clinically detectable muscle weakness).

3. • Fatigue is subjective term reported by patient as weakness-like
complain felt after exercise but actually muscle power is
normal,
i.e: no pathology in muscle or in its nerve supply. So fatigue is
non- objective muscle weakness, non-neuromuscular
weakness, functional muscle weakness or false muscle
weakness.
Motor Nerve
Supply
3
True Muscle
Weakness Wrong neither
in muscle nor
in its nerve
supply
Function
al
Muscle
weaknes
s
[Myopathy
]
Muscl
e

4. 4
Why approach to weakness is very
important?
• Because stroke enter in differential diagnosis of weakness
which severe condition & current stroke management
mandates urgent evaluation of unilateral limb weakness.

5. 5
Classification by Algorithm-wise
Approach:
First of all keep in your mind the following helping questions:
• Mode of Onset & Duration:
oAcute: vascular, toxic & metabolic.
oChronic: neoplastic, infective, inflammatory, endocrine,
degenerative diseases.
• Course:
oWorse at onset then get regress later on: neurogenic cause:
vascular.
oProgressive: neurogenic cause: neoplasm, degenerative & infective
diseases.
oEpisodic: neurogenic cause: vascular.
oActivity dependent: NMJ cause: MG & muscular cause: myopathies.

6. 6
o UMNL or LMNL signs.

7. 7
Reviews:
Stroke:
•Most common cause of unilateral weakness.
•Patients typically present with sudden onset of
the complains.
•If persist < 3 hours , then it will resolve (TIA),
while if persist > 3 hours, then it will not resolve
(true stroke).
•It can be cortical ,subcortical, brainstem or spinal

8. •How to approach stroke.
1. Identify nature
whether ischemic or hoemorrhagic. If
ischaemic then embolic or thrombotic.We have to ask
three question,1. time of stroke, 2.deficit at onset and
3.progression.
Thrombotic stroke usually occurs at 4 am, while embolic
and heomorrhagic usually during activity.
Embolic give rise to fixed deficit but deficit progresses in
thromotic.

9. LOCALIZATION
 2. Site/localization. Before localization try to understand some words
 The words are.
1. Hemilegia vs hemiparesis
2. Dense hemiplegia,brachial (upper limb more weaker than lower limb)
and crural (lower limb more weaker than upper limb) hemiplegia.
3.crossed (cranial nerve manifestation on one side and hemiplegia on
other side) and uncrossed hemiplegia (both cranial nerve manifestation
and hemiplegia on same side)

11. All cranial nerves has dual/bilateral supply from
hemispheres except some part of facial and some
part of hypoglossus

12. • Now how to say that stroke is cortical,
The hemiplegia will be either crural or brachial and
there may be cortical dysfunction as mentioned below
1
2

13. -How to say internal capsule.
Answer is dense hemiplegia. No cortical
sign.
-Qustion, which site is more common for
thrombotic, cortical or internal capsule?
-How to say subcortical stroke??

14. Space-occupying lesions (SOL):
e.g. tumors, abscesses, chronic subdural
hematoma, can cause symptoms & signs
mimicking stroke but the onset is
typically more gradual
& progressive.
•There may be
features of raised
ICP.
10

15. Brainstem stroke. (midbrain)

16. Other midbrain syndromes
 Perinaud.
 Claude
 Nothnagel
 benedict

17. Pontine syndrome

18. Medullary syndrome

19. Pseudobulbar vs bulbar palsy

20. can spinal cord lesion manifest as
hemiplegia
 Yes, if hemicut above c5

21. 11
Spinal cord lesions:
•Above level of C5:
oHemicut: Ibsilateral UMN hemiparesis/ hemiplegia and
deep hemiparesthesia with contralateral superficial
hemiparesthesia.
oComplete cut: UMN quadriparesis/ quadriplegia with
bilateral loss
all sensation types.
N.B: If injury involve C3, C4 & C5, then patients will
be died (because these are root values of phrenic
nerve).
•C5 to T1 (brachial plexus):
oHemicut: ibsilateral LMN hemiparesis/ hemiplegia and deep
hemiparesthesia with contralateral superficial
hemiparesthesia in upper limbs & ibsilateral UMN
hemiparesis/ hemiplegia and deep hemiparesthesia with
contralateral superficial hemiparesthesia in lower limbs.

22. 12
o Complete Cut: bilateral LMN weakness with bilateral
loss of all sensation types in upper limbs & bilateral UMN
weakness with bilateral loss of all sensation types in
lower limbs.
•T2 to L1:
oHemicut (Brown Sequard syndrome): ibsilateral UMN or
LMN monoparesis/ monoplegia in lower limb with ibsilateral
deep sensory loss & contralateral sensory loss take sensory
level pattern on trunk & autonomic dysfunction symptoms.
oComplete cut: UMN (spastic) paraparesis/ paraplegia or
LMN (flaccid) paraparesis/ paraplegia with or without
sensory loss take sensory level pattern on trunk &
autonomic dysfunction symptoms.

23. 13

24. 14
•Below L1 (Lumbosacral Plexus/ Cauda-Equina):
always LMN weakness in lower limbs unilaterally or bilaterally
but not to similar extent with sensory loss take “glove &
stocking” pattern & autonomic dysfunction symptoms.

25. By the way: 15

26. Multiple Sclerosis (MS):
16
•Idiopathic inflammatory demyelinating disease of
white matter of the brain and spinal cord.
•Common in women between 20 – 40 years.
•Usually monosymptomatic.
•Characterized by relapsing & remitting course.
•Presented with motor, ocular sensory, cerebellar,
autonomic or cranial nerves abnormalities. The
ocular abnormality is the most common one.
•Can presented with almost any pattern of UMN
limb weakness, though paraparesis secondary
to TM is the most typical.

27. AHC Lesions; Motor Neuron Diseases (MND):
17
•It’s group of chronic degenerative diseases of
unknown
etiology affecting the motor system only.
•Characterized by gradual onset and progressive
weakness.
•Common in males > 50 years.
•Affect UMN or LMN or both. Can be presented with
bulbar symptoms.
•No sensory, cerebellar, autonomic or ocular
abnormalities.

28. Peripheral nerve lesions:
• Cause LMN limbs weakness.
• Can be caused by:
o Metabolic causes: DM, Renal failure, Hypoglycemia.
o Inflammatory causes: GBS, Sarcoidosis, Chronic
Inflammatory Demyelinating Polyradiculoneuropathy
(CIDP).
o Toxins: Botulism, Lead, Alcohol.
o Vasculitis: RA, PAN, Wegener’s granulomatosis.
o Drugs: INH, Phenytoin, Cisplatin.
o Congenital: Charcot Marie Tooth disease.
18

29. Guillain-barre Syndrome: 19
•It is acute ascending inflammatory
demyelinating polyneuropathy that
is autoimmune in nature.
•Can affect any age.
• Presentation is acute.
• H/O URTI, diarrhea,
vaccination 2 weeks before
the presentation.
• Symmetrical ascending
weakness of regressive course.
• Dyspnea is alarming sign.

30. 20
NMJ lesions; Myasthenia Gravis (MG):
•Autoimmune neuromuscular disorder
characterized by fatigable LMN muscle
weakness.
•Common in women between 20 – 40 years.
•Type of weakness is fatigable & of diurnal variation,
i.e: muscle power initially is normal then get
weakens with repeated activity to became true
weakness at end of day.
•Associated with ocular & bulbar symptoms & tend
to be affected before limb muscles.
•Occur as relapsing & remitting course

31. Muscle Lesions; Myapathies (Proximal LMN
weakness):
21
• Inflammatory Myopathy: polymyositis, dermatomyositis, vasculitis.
• Infectious Myopathy:
o Bacterial: pyomyositis, Lyme myositis.
o Viral: influenza, parainfluenza, Coxsackie, HIV, CMV, echovirus, adenovirus, EBV.
o Fungal infections.
o Parasitic: trichinosis, toxoplasmosis.
• Drug/Toxic Myopathy: steroid, alcohol, cocaine, heroin, colchicine, antimalarial,
statins, fibrates, penicillamine, zidovudine, gemcitabine.
• Endocrine Myopathy: hypothyroidism, hyperthyroidism, Cushing’s, diabetes,
acromegaly.
• Metabolic Myopathy: hypokalemia, hypocalcemia, hypophosphatemia,
hyponatremia,
hypernatremia, disorders of carbohydrate/ lipid/ purine metabolism.
• Neoplastic Myopathy: paraneoplastic syndrome.
• Rhabdomyolysis:
o Drugs: alcohol, cocaine, statins, neuroleptic malignant syndrome, malignant hyperthermia.
o Hyperactivity: seizures, exertion.
o Trauma/ Operation.

32. Remember that: 22
•Muscle Power: preserved in patients with cachexia
despite advanced generalized muscle atrophy. In
contrast, patients with true muscle weakness due to
myopathy have low muscle power generally have
normal muscle bulk at time of presentation.
•Muscle Tenderness: usually not associated with one
of the causes of true muscle weakness, except for
infectious myopathies, certain drug- induced
myopathies, rhabdomyolysis, thyroid myopathy, and
inherited metabolic myopathies.

33. Diagnosis By
Algorithm-
wise
Approach:
Patient complain
of weakness
Is the weakness,
true?
Is the true weakness
is strictly
unilateral?
Unilateral
weakness
Do blood
sugar
test
This mean cortical
stroke excluded by far
extent & lesion is in
spinal cord
(paraparesis/
paraplegia)
Is the onset,
sudden?
Is it associated with features of acute limb
ischemia (pain, cold, pale, mottled skin &
absent pulse)?
Request vascular
surgeon
consultation
Urgent Spine
MRI
• Cord compression
• Intrinsic spinal cord pathology
(Syringomyelia, TM, glioma,
abscess)
Immobilize patient
& do cervical
spine image if
there is h/o
trauma
Severe back pain +
sparing of proprioception
& vibration?
Request neurosurgeon
or oncologist
consultation
Spinal
infarction
Are there UMN
signs?
Is it associated with
sensory level & sphincter
disturbance?
Is there MRI
evidence
of
myelopathy?
• Cord compression
• Intrinsic spinal cord pathology
(Syringomyelia, TM, glioma,
abscess)
• SCDD
(plasma
vitamin B12)
• Post-
radiotherapy
myelopathy
(Hx)
• MND; ALS (Hx
&
Ex)
Bilateral intracranial
lesions: cerebral
emboli/ metz, venous
stroke, demyelination/
MS (Hx & Ex and brain
image)
This is mean LMN
signs
Are there sensory
s/s?
Peripheral
neuropathy (distal
weakness):
GBS (Hx, Ex, NCS,
LP,
vital capacity monitor)
Refer to neurologist
CIDP (Hx, Ex, NCS,
FBS,
HIV test, urinary
porphyrin,
serum protein
electrophoresis)
Refer to neurologist
Bilateral
radiculopathy (Hx,
Ex, spinal cord
image)
Refer to neurologist
Otherwise:
• Ask about drugs/ alcohol Hx, family Hx of
charcot’s disease, social Hx of lead exposure
…etc
• Request following Ix: FBC, BS, U,E&C,
ESR, CRP, Ca, RF, TFT
Is there muscle
fatigability (fatigable/
post-exercise
weakness)?
Tendon reflexes?
MG (Hx, Ex,
tensilon test,
EMG, anti-
Ach receptor
AB, thoracic
CT)
LEMS (anti-
voltage-
gated
calcium
channels
AB, EMG,
screen
underlying
malignancy)
Proximal
weakness
?
Myopathies
Hx: bedridden patient, drugs/
alcohol hx, past medical hx,
past surgical hx, h/o trauma
…etc
Ix: FBC, U,E&C, ESR, CRP,
BS, Ca, RF, TFT, CK,
EMG • Infective myopathy (FBC, ESR, PCT)
• Some drugs induced myopathy (statin)
• Myositis; polymyositis,
dermatomyositis (anti-synthetase
AB)
• Insist on considering peripheral neuropathy, MND, mononeuritis multiplex,
myopathies, generalized weakness secondary to acute illness, functional
weakness.
• Refer to neurologist if no cause identified.
Ye
s
Functional weakness
(fatigue)
No
Ye
s
Ye
s
No
Ye
s
No
Ye
s
Ye
s
No
Ye
s
No
Ye
s
No
Ye
s
No
No
No
Ye
s
Absen
t
Normal
Ye
s
No
No
Is there weight
Loss?
Is there
pallor?
Anemia
s
MG
Drugs/ alcohol
Hx?
• Alcohol
• Cocaine
abuse
• Chronic
aspirin
ingestion
• Anxiety
• Depression
• Fibromyalgia
• Aldosteronism
Is there fever?
• TB
• SBE
• Collagen
diseases
• Other infections
Neurologic
findings?
Is there
Polyuria?
• Hyperthyroidism
• DM
• DI
• Hyperparathyroidism
• CKD
• Electrical
disturbances
• Neoplasm
• Malnutrition
• Addison’s disease
• Cirrhosis
• Malabsorption syndrome
• CHF
• Parkinson’s
disease
• Muscular
dystrophy
• MND (ALS)
• MS
• Neuropathies
No Yes
No Ye
s
Is the fatigue
constant?
Yes No
+ve -ve
Ye
s
No
-ve
+ve
No
Ye
s
Is the onset,
sudden?
Is it
painful
?
Ischemia (compare pulse &
capillary refilling between 2
limbs)
Refer to vascular
surgeon
Fracture (Hx of trauma & do X-
ray)
Refer to orthopedist
Compartment syndrome (CK
level in blood)
Stroke TIA
Are there seizure,
evidence of increased
ICP, cortical
dysfunction or CNS
infection?
• SOL
• Meningoencephaliti
s (fever, purpuric
skin rashes &
meningeal irritation
signs)
• LP
• Neuroimage
Are there UMN
signs?
Is there contralateral sensory
loss?
Unilateral spinal cord
lesions
MRI
Spine
• Ipsilateral sensory loss: SOL, stroke,
MS
• Normal sensation: MND
Is signs are referable
to single nerve root/
single nerve?
Radiculopathy or mononeuropathy
• Insist on considering plexopathy, multi-root
compression, MND, stroke, migraine, functional
weakness.
• Refer to neurologist if no cause identified.
Ye
s
Ye
s
Is duration > 3 hours?
Yes No
No
Ye
s
No
Ye
s
Ye
s
No
No
No
Ye
s
MRI
Spine
Ye
s No
Muscle
Tenderness
No
Other myopathies
Ye
s
No
MotorCortex
Spinal
Cord
Peripheral
Nerves
NM
J
Muscle
Bilateral True
Weakness
Unilateral True
Weakness
Functional
Weakness
23

34. cases

35. Sources: 24
• Macleod's Clinical Diagnosis 2nd Ed (2013)
• Approach to Internal Medicine 4th Ed (2015)
• Algorithmic Diagnosis of Symptoms and Signs 4th Ed
(2017)
• Toronto Notes 34th Ed (2018)
• Ain-Shams University Internal Medicine curriculum
(2014)
• Decision Making in Medicine 3rd Ed (2010)

36. THANK
YOU
25