WEAKNESS

• WEAKNESS
• Weakness is a reduction in normal power of
one or more muscles.
• Limitation in rising from a seated position or
combing hair suggests proximal weakness,
whereas slapping of the feet while walking or
limitation in opening jars suggests distal
weakness.
• The suffix “-plegia” indicate weakness that is
so severe that it is complete or nearly
complete. “Paresis” refers to weakness that is
mild or moderate. The prefix “hemi-” refers to
one half of the body, “para-” to both legs, and
“quadri-” to all four limbs.
• Tone is the resistance of a muscle to passive
stretch. Central nervous system (CNS)
abnormalities that cause weakness generally
produce spasticity
• Spasticity an increase in tone due to upper
motor neuron disease. Spasticity is velocity-
dependent, has a sudden release after
reaching a maximum (the “clasp-knife”
phenomenon), and predominantly affects
antigravity muscles (i.e., upper limb flexors
and lower limb extensors). Spasticity is distinct
from rigidity other types of increased tone..
• Rigidity is increased tone that is present throughout the
range of motion (a “lead pipe” or “plastic” stiffness) and
affects flexors and extensors equally. In some patients,
rigidity has a cogwheel quality that is enhanced by
voluntary movement of the contralateral limb
(reinforcement). Rigidity occurs with certain
extrapyramidal disorders such as Parkinson's disease.
Weakness with decreased tone (flaccidity) or normal
tone occurs with disorders of the motor unit, that is, a
single lower motor neuron and all of the muscle fibers it
innervates
• Three basic patterns of weakness can usually be
recognized based on the signs summarized. One
results from upper motor neuron pathology, and the
other two from disorders of the motor unit (lower
motor neuron and myopathic weakness).
Fasciculations and early atrophy help to distinguish
lower motor neuron (neurogenic) weakness from
myopathic weakness. A fasciculation is a visible or
palpable twitch within a single muscle due to the
spontaneous discharge of one motor unit
TABLE 21-1 Signs That
Distinguish Patterns of
Weakness

Sign Upper Motor Neuron Lower Motor Neuron

Atrophy None Severe

Fasciculations None Common
Tone Spastic Decreased
Distribution Pyramidal/regional Distal/segmental
ofweakness
Tendon reflexes Hyperactive Hypoactive/absent
Babinski's sign Present Absent
Hemiparesis
• Definition :
• Hemiparesis, or unilateral paresis, is weakness
of one entire side of the body (hemi- means
"half"). Hemiplegia is, in its most severe form,
complete paralysis of half of the body. The
most common cause of hemiparesis and
hemiplegia is stroke.
• Common causes
• Vascular: cerebral hemorrhage, stroke, cerebral palsy
• Infective: encephalitis, meningitis, brain abscess, cerebral palsy, spinal epidural abscess
• Neoplastic: glioma, meningioma, brain tumors, spinal cord tumors
• Demyelination: multiple sclerosis, disseminated sclerosis, ADEM, neuromyelitis optica
• Traumatic: cerebral lacerations, subdural hematoma, epidural hematoma, cerebral palsy, 
vertebral compression fracture
• Iatrogenic: local anaesthetic injections given intra-arterially rapidly, instead of given in a
nerve branch.
• Ictal: seizure, Todd's paralysis
• Congenital: cerebral palsy, Neonatal-Onset Multisystem Inflammatory Disease (NOMID)
• Degenerative: ALS, corticobasal degeneration
• Parasomnia: sleep paralysis[13]
• Hemiparesis site of lesion : .
• A “pure motor” hemiparesis of the face, arm, and/or leg is
due to a small, discrete lesion in the posterior limb of the
internal capsule, cerebral peduncle, or upper pons .The
absence of cranial nerve signs or facial weakness suggests
that a hemiparesis is due to a lesion in the high cervical
spinal cord, especially if associated with ipsilateral loss of
proprioception and contralateral loss of pain and
temperature sense (the Brown-Séquard syndrome).
However, most spinal cord lesions produce quadriparesis or
paraparesis.
corticospinal tract
• is recognized by various accompanying features.
Motor cortex. Weakness and/ or loss of skilled
movement confined to one contralateral limb (an
arm or a leg - monoplegia) or part of a limb (e.g. a
weak hand) is typical of an isolated motor cortex
lesion (e.g. a secondary neoplasm). A defect in
higher cortical function (e.g. aphasia) and focal
epilepsy may occur.
• Internal capsule.
• Since all corticospinal fibres become tightly
packed as they reach the internal capsule,
occupying about 1 cm2 , a small lesion causes
a large deficit. For example, an infarct of a
small branch of the middle cerebral artery
causes a sudden, dense, contralateral
hemiplegia.
• brainstem.
• Some brainstem lesions produce “crossed
paralyses,” consisting of ipsilateral cranial nerve
signs and contralateral hemiparesis pontine lesion
(e.g. a plaque of multiple sclerosis) is rarely
confined only to the corticospinal tract. Since
adjacent structures such as the sixth and seventh
nuclei, MLF and PPRF are involved, there are other
localizing signs - VI and VII nerve palsies
•Stroke
• Definition :
• Stroke is characterized by the sudden onset a focal neurologic impairment
that stroke can be further subdivided into ischemic and hemorrhagic stroke.
• Hemorrhagic stroke has two further subtypes:
• subarachnoid hemorrhage (SAH), which is usually caused by rupture of an
intracranial aneurysm, and nontraumatic intracerebral hemorrhage (ICH).
• Ischemic stroke
• can be further classified as lacunar (a small subcortical infarct), large artery
atherosclerotic (either intra or extracranial), cardioembolic, or cryptogenic.
• Transient Ischemic Attack
• (TIA) is defined by transient focal neurologic symptoms resulting from
brain, retinal, or spinal cord ischemia and was initially defined as lasting
less than 24 hours. A more recently Neurology adopted definition
recognizes the high prevalence of acute infarcts on neuroimaging and
emphasizes that TIA is defined by the absence of infarction on
neuroimaging, independent of symptom duration. TIA symptoms typically
are short lasting, usually 5 minutes to 1 hour, and include sudden-onset
hemiparesis, hemisensory loss, change in speech function (either aphasia
or dysarthria), loss of vision, or inability to walk. Patients with a suspected
TIA should thus undergo neuroimaging with either noncontrast MRI or CT
within 24 hours of the onset of neurologic deficits.
• TIA is considered a neurologic emergency given the subsequent 48-hour
and 90-day risk of ischemic stroke.
• Causes :
• cardioembolic stroke
• The most common cause of cardioembolic stroke is atrial
fibrillation.
• calcific mitral stenosis
• ventricular thrombus
• internal carotid artery atherosclerosis
• autoimmune and hypercoagulable disorders
can be considered in young patients with otherwise
unexplained stroke
 Onset & progress:
thrombotic
• Most common
• Onset during sleep or on arising
• Usually in elderly
• Stepwise evolution
• Gradual recovery
• Evidence of atherosclerosis
• Hx of TIA may be found
 Embolic:
• Abrut with complet stroke within seconds
• Hx of heaert disease
• Occure in any age
• Localized headache or seizure
• Rapid recovery
• No Hx of TIA
• Hemorregic:
• Hx of HTN
• Onset during walking hours
• Headache , seizure, vomiting & coma may
associate
• Nuchal rigidity
• Subacute hemiparesis that evolves over days or weeks has an
extensive differential diagnosis. A common cause is subdural
hematoma; this readily treatable condition must always be
considered, especially in elderly or anti coagulated patients,
even in the absence of a history of trauma. Infectious
possibilities include cerebral bacterial abscess, fungal
granuloma or meningitis, and parasitic infection. Weakness
from primary and metastatic neoplasms may evolve over days
to weeks. AIDS may present with subacute hemiparesis due to
toxoplasmosis or primary CNS lymphoma. Noninfectious
inflammatory processes, such as multiple sclerosis or, less
commonly, sarcoidosis, are further considerations.
• Chronic hemiparesis that evolves over months
is usually due to a neoplasm, an unruptured
arteriovenous malformation, a chronic
subdural hematoma, or a degenerative
disease. The initial diagnostic test is often an
MRI of the brain, especially if the clinical
findings suggest brainstem pathology.
• Acute Stroke managment
• The initial therapy in acute stroke depends on
whether the stroke is ischemic or
hemorrhagic. Regardless of stroke etiology, a
primary goal of hospitalizing all affected
patients is the prevention and treatment of
associated medical and neurologic
complications.
• A focused history and physical examination
• measurement of blood glucose level
• rapid imaging with noncontrast head CT is required
to exclude ICH. complete blood count
• coagulation profile
• basic metabolic profile.
• ECG-ECHO
• Cartid doppler
• ANA profile (young pt)
• Blood glucose, hydration, oxygen saturation and temperature should
be maintained within normal limits
• Blood pressure should not be lowered in the acute phase unless there
are complications e.g. Hypertensive encephalopathy.
• Aspirin 300mg orally or rectally should be given as soon as possible if a
haemorrhagic stroke has been excluded.
• With regards to atrial fibrillation, the RCP state: 'anticoagulants should
not be started until brain imaging has excluded haemorrhage, and
usually not until 14 days have passed from the onset of an ischaemic
stroke'.
• If the cholesterol is > 3.5 mmol/l patients should be commenced on a
statin. Many physicians will delay treatment until after at least 48 hours
due to the risk of haemorrhagic
• Thrombolysis should only be given if:
• It is administered within 4.5 hours of onset of
stroke symptoms (the thrombolytic window)
(unless as part of a clinical trial). 
Haemorrhage has been definitively excluded
(i.e. Imaging has been performed).  Alteplase
(tPA) is currently recommended by NICE
EX: PT WITH ISCHEMIC STROKE: AT
DISCHARGE FROM HOSPITAL AFTER 14
DAYS >> HE SHOULD
RECEIVE: (CLOPIDOGREL + STATIN IF THE
CHOLESTEROL IS > 3.5).
Paraparesis
• This term refers to impairment or loss of
motor and/or sensory function in the thoracic,
lumbar or sacral (but not cervical) segments of
the spinal cord, secondary to damage of neural
elements within the spinal canal. With
paraplegia, arm functioning is spared, but,
depending on the level of injury, the trunk,
legs and pelvic organs may be involved.
• Paraparesis
• An intraspinal lesion at or below the upper thoracic
spinal cord level is most commonly responsible. A
sensory level over the trunk identifies the approximate
level of the cord lesion. Paraparesis can also result from
lesions at other locations that disturb upper motor
neurons (especially parasagittal lesions and
hydrocephalus) and lower motor neurons (anterior horn
cell disorders, cauda equina syndromes, and
occasionally peripheral neuropathies).
• When injury to the corticospinal tracts occurs,
spastic paresis or paralysis is possible,
manifesting as weakness, hyperreflexia, muscle
spasms, and extensor plantar responses.
• Involvement of the distal spinal cord and lower
roots (cauda equina syndrome) can involve
weakness of the lower motor neuron type, with
decreased muscle tone and areflexia
• Classification:
• Spastic paraparesis
• Flaccid paraparesis
• Spastic paraparesis
• With sensery level: causes
• -cord compression:
• 1/ potts disease
• 2/ disc prolapse
• 3/mets
• 4/ epidural tumor, abscess, or hematoma
-Transverse myelitis
-Anterior spinal artery occlusion
-MS (Recurrent episodes )
• Spastic paraparesis
• Without sensery level: causes
• MND
• Hereditary spastic paraparesis
• Tropical spastic paraplesia
• Parasagittal tumors
• MS
• SACDC
• Syringomyelia
• Infection(HIV,Neurosyphilis,neurobrucellosis)
• Flaccid paraparesis
• Causes:
• Guillian-baree synd
• CIDP
• Charcot marie tooth
• Periodic hypokalaemic paralysis
• Polio(old) ,unilatral
• Investigation:
• MRI spine
• Blood tests CBC ESR CRP
• PSA
• PROTEIN ELECTROPHORESIS
• SCREENING FOR TB(CXR , Mantoux)
• SCEEENING FOR METS
• CSF for oligoclonal band(MS)
• Vit B12
• Viral sceening
• NCS
 Transverse myelitis
• It is an inflammatory lesion that can affects
the cord. Constitutional symptoms such as
headache and fever are common as is pain.
Signs are indistinguishable from those caused
by cord compression and again all sensory
aspects are equally affected with no sparing of
proprioception..
• The clinical signs are caused by an interruption in
ascending and descending pathways in the
transverse plane of the spinal cord. A sensory
level is characteristic. Midline or dermatomal
neuropathic pain can be present. Urinary
incontinence or retention, bowel incontinence or
constipation, and sexual dysfunction are common
but vary in severity. These signs develop over
hours to days, and are usually bilateral.
• There are a variety of causes, but it most often
occurs as an autoimmune
phenomenon(idiopathic )after an infection or
vaccination, or (nonidiopathic )as a result of
direct infection (herpes simplex virus, varicella
zoster, West Nile virus, human T-lymphotropic
virus, Lyme disease, and neurosyphilis. HIV)
• For a significant proportion of cases no cause is
found.
• MRI is indicated to rule out the presence of
structural lesions, and determine the presence
of myelitis which enhances with gadolinium in
the acute phase. There may be more than one
area of myelitis, and the lesions usually span
at least two vertebral segments. In the acute
phase the MRI may be normal.
• Treatment in the acute phase aims to halt the
progression and initiate resolution of the
inflammatory cord lesion. High doses
Corticosteroids IV are first line. Plasma
exchange can be given to those who fail to
respond. Patients with demyelinating disease
can be started on long term
immunosuppression
• Subacute Combined Degeneration of spinal cord (SCD) :
• (Lichtheim’s disease). It refers to degeneration of the posterior and lateral columns of
the spinal cord as a result of Vit B12 deficiency (most common), Vit E deficiency or
Friedrich’s ataxia. It is usually associated with pernicious anaemia.
• Features:
•  Patchy losses of myelin in the dorsal and lateral columns.
•  Present with progressive weakness of legs, arms, trunk, tingling and numbness.
•  Visual and mental changes may also be present.  Bilateral spastic paresis with
diminished pressure, vibration and touch sense.  Positive Babinski sign may be seen.
•  Extensor plantars with absent ankle reflexes Prolonged deficiency of Vit B12 (>3
months) leads to irreversible nervous system damage. If someone is deficient on Vit
B12 and folic acid, the Vit B12 deficiency should be treated first to avoid precipitating
SCD of the cord
• TTT with Vit B12 results in partial to full recovery, depending on the duration and
extent of neurodegeneration.