PARAPARESIS
May25, 2020
PRESENTED BY : SHALVI
ROLL NO. - 149
8TH SEMESTER
I've been given this case data to solve in an attempt to understand and analyize the topic "PARAPARESIS" based on patient clinical data in order to develop competency in reading and comprehending clinical data related to Paraparesis and come up with a suitable diagnosis.
You can refer to the case at
UNDERSTANDING THE CASE
Patient suffers from bilateral symmetrical lower limb weakness and bilateral edema in both the legs
1] WEAKNESS IN BOTH LEGS
There is no weakness in the upper limbs and there is no cranial nerve involvement
Weakness in bilateral lower limbs started 2 yrs ago. It started as a proximal muscle weakness and over the years has now progressed to a distal weakness.Proximal muscle weakness since difficulty in squatting and getting up from that position. Distal muscle weakness suggested by difficulty in wearing and holding chappals.The weakness is insidious in onset and is gradually progressive in nature.
2) EDEMA IN BOTH LEGS
It is of non pitting type
Medical history:
Not a known case of hypertension, diabetes mellitus, epilepsy, thyroid.
Family history :
Not significant
Personal history:
Diet -mixed
Appetite - normal
Sleep- adequate
Bowel and bladder movements - regular
Drug history :
The patient has no known drug allergies or use of any drugs.
GENERAL EXAMINATION-
-patient was conscious, coherent and coperative
-moderately built and nourished.
-no signs of pallor, icterus, clubbing, cyanosis, lymphadenopathy, edema
-VITALS
1.temperature-AFEBRILE
2.pulse rate-92bpm
3.respiratory rate-18 cycles/min
4.BP-130/90mmhg
5.SpO2-96%
6.GRBS-142mg/dl
SYSTEMIC EXAMINATION
1. CVS-
S1 S2 heard
no added murmurs
2.RESPIRATORY SYSTEM-
-normal vesicular breath sounds heard
-bilateral air entry present
3.PER ABDOMEN-
shape=scaphoid
umbilicus=central and normal in position
all quadrants moving equally on respiration
no tenderness
no organomegaly
bowel sounds-heard
no bruit heard
2.RESPIRATORY SYSTEM-
-normal vesicular breath sounds heard
-bilateral air entry present
3.PER ABDOMEN-
shape=scaphoid
umbilicus=central and normal in position
all quadrants moving equally on respiration
no tenderness
no organomegaly
bowel sounds-heard
no bruit heard
4.CNS-
higher mental functions= normal
Cranial nerves- intact
Motor system-
tone - normal
power - 4-/5 in both lower limbs
reflexes absent in both lower limbs
sensory system-normal
No meningeal signs
No cerebellar signs
DIFFERENTIAL DIAGNOSIS
1. Weakness -
It can be Upper Motor Neuron or Lower Motor Neuron Disease
Features of upper motor neuron lesion are:
- Spasticity
- Hypertonicity
- Hperreflexia
- Disuse atrophy (minimal)
- Positive babinski's sign
Features of lower motor neuron lesion are:
- Flaccidity
- Hypotonicity
- Hyporeflexia
- Denervation atrophy(profound)
- Negative babinski's sign
- Fasciculations are present
In this patient there are no features suggestive of upper motor neuron lesion.
It can be either upper motor neuron or lower motor neuron. Since the patient has absence of reflexes, absence of any fasiculations, twitches and he has intact sensations therefore he can have a lower motor neuron lesion.
- Anterior horn cell disease
- Nerve root ( radiculopathy)
- Plexus injury ( pain with sensory loss)
- Peripheral nerve disease
- Neuromuscular junction
- Muscle
ANTERIOR HORN CELL
- There is no sensory , autonomic or cerebellum involvement
- Affects distal muscles
- There are fasciculations , wasting
- It has asymmetrical onset
RADICULOPATHY
- Usually Asymmetrical
- Root pain is present along the distribution of nerve.
- Sensory,motor systems involved and areflexia seen.
- Muscles supplied by that particular nerve root are involved.
PERIPHERAL NERVE DISEASE
- Motor and sensory involvement is seen
- There is distal to proximal evaluation
They can be AXONAL or DEMYELINATING neuropathies.
AXONAL NEUROPATHY
It is a chronic polyneuropathy with distal to proximal evolution.Reflexes are usually spared unless it is a large fibre neuropathy.
There is predominant sensory involvement.
DEMYELINATING NEUROPATHY
It has a acute to subacute presentation and is a polyradiculoneuropathy.
There is diffuse proximal and distal muscle involvement.
Reflexes are lost.
There is predominant motor involvement.Sensory system if involved is mainly dorsal column involvement.
NEUROMUSCULAR JUNCTION
- There is fatiguability
- There is fluctuating weakness
- There is ocular and pharyngeal muscle involvement
MUSCLE
- There is only motor involvement
- It has symmetrical onset
- There is predominantly proximal muscle involvement
- There is no wasting
- Reflexes are preserved
- There are no fasciculations
FROM THE ABOVE DISCUSSION WE CAN CAN COME TO THE CONCLUSION THAT THE DIFFERENTIAL DIAGNOSIS CAN BE:
1) MYOPATHY
2)DEMYELINATING POLYNEUROPATHY
MYOPATHY
Myopathy refers to a clinical disorder of the skeletal muscles causing weakness of muscle. Abnormalities of muscle cell structure and metabolism lead to various patterns of weakness and dysfunction. In some cases, the pathology extends to involve cardiac muscle fibers, resulting in a hypertrophic or dilated cardiomyopathy.
Disruption of the structural integrity and metabolic processes of muscle cells can result from genetic abnormalities, toxins, inflammation, infection, and hormonal and electrolyte imbalances.
IT CAN BE INTERMITTENT OR PERSISTENT WEAKNESS SINCE IT IS A CASE OF CONSTANT WEAKNESS IT CAN BE CLASSIFIED AS
It can be further classifies into INHERITED or AQUIRED Myopathy
Inherited muscle disorders are called muscular dystrophies:
- Duchenne's muscular dystrophy
- Becker's muscular dystrophy
- Limb girdle muscle dystrophy
- Emery Dreifuss muscle dystrophy
- Fascioscapulohumeral muscle dystrophy
- Myotonic dystrophy
- Mitochondrial myopathies
Dystrophinopathies(Duchenne and Becker's) are likely in this case.
- Both have X-linked recessive inheritance due to a mutation in dystrophin gene.
- Duchenne muscular dystrophy is a more severe form usually presenting before the age of 5. Proximal muscles of lower limbs are predominantly involved with positive gower's sign There is pseudohyperthrophy of calf muscles.They do not live longer because of serious cardiac conduction abnormalities and dilated cardiomyopathy.Therefore,Duchenne is unlikely in this patient.
- Becker's usually survive into their 40's and have highly variable disease onset.
Acquired myopathies are due to the following causes:
- Inflammatory (Polymyositis/Dermatomyositis)
- Drug induced
- Endocrine
FURTHER INVESTIGATIONS REQUIRED:
- Electromyography
- Genetic testing
- Creatinine phosphokinase levels;Increased in dystrophie
- Nerve conduction study:Demyelinating neuropathies show slowing of conduction velocities, prolongation of distal latency
- Muscle biopsy
TREATMENT:
Presently there is no cure for muscular dystrophy.
- Corticosteroids- increase muscle strength and slow progression
- Heart medications if associated with any heart conditions
- Physiotherapy
- ACE INHIBITORS/ ARB’s and Beta blockers to treat cardiomyopathy
Following are my reference:
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