⭐⭐ PARAPLEGIA ⭐⭐

              ⭐⭐ PARAPLEGIA ⭐⭐

1) DEFINITION OF PARAPLEGIA :- 

    Paraplegia is paralysis of both lower

   limbs. 

  - Paralysis - complete or partial

    loss of muscle function leading to loss

    of ability to move.

  -  The loss of muscle function occurs

     when there is damage to its nerve               supply.

  - The motor pathway innervating the               muscles consists of Upper motor 

     neuron (UMN) and lower motor neuron

     (LMN).

  - The UMN originate in the cerebral                 cortex and travel down to  the brain             stem or spinal cord to the level of                 appropriate spinal nerve root .At this           point,  the lower  motor neurons begin         in the anterior horn of spinal cord and         goes to innervate muscles and                     glands throughout the body.

  - The nerves of lumbosacral spinal cord

     supplies the lower limbs. Damage to

    this part leads to paraplegia.

   ⭐⭐ JUST FOR INFORMATION :- ⭐⭐

    Neuromuscular transmission :- 

    (a) Action potential in the nerve ending 

        causes depolarisation.

    (b) This depolarisation causes influx of

        calcium ions in the motor neuron 

        terminal.

    (c) This leads to fusion of vesicles 

        containing acetylcholine with the 

        pre synaptic membrane . Emptying

        of these vesicles causes release of

        neurotransmitter acetylcholine in the

        synapse.

    (d) Acetylcholine binds to the receptors

        present on the post synaptic                          membrane.

    (e) This binding leads to generation of

        end plate potential. This end plate

        potential when reaches threshold,

        leads to generation of Action                        potential by influx of sodium.

    (f) This action potential leads to muscle

        contraction by a process called

        excitation contraction coupling .

        

2) CAUSE OF PARAPLEGIA :- 

   It mainly occurs due to damage to               spinal cord.

   But , sometimes it may also be caused

   due to damage to brain or peripheral

   nerves or muscle involvement.

   (A) Spinal cord related causes :-

       (I) Acute paraplegia :- 

          # Trauma to the spinal cord - leads 

           to damage to nerves supplying

           lower limb.

          # Spinal cord infarction due to

             - Vasculitis (Inflammation leads to

             damage to the vessel supplying 

             spinal cord, thus impairing the 

             blood supply.)

            - Anterior spinal artery thrombosis

            

          # Transverse Myelitis (It is sensory,

             motor or autonomic dysfunction

             due to Inflammation of spinal cord

             i.e. Myelitis at a level of cord) 

             - Inflammation may occur due to                     various causes like:

               Autoimmune diseases.

               Sarcoidosis.

               Vasculitis.

               Certain drugs like Cisplatin.

               Post vaccine disease.

               Idiopathic etc.

           # Neuromyelitis optica 

             - It is an autoimmune                                         inflammatory disease which 

               causes damage to the myelin 

               sheath of neurons. This affects

               the neuronal conduction.

            # Multiple sclerosis

              - It is an autoimmune                                        inflammatory disease which 

               causes damage to the myelin 

               sheath of neurons. This affects

               the neuronal conduction.

        (II) Chronic or Subacute paraplegia:-

            Lesion can be present in

            following spaces: 

             # Extradural cause :- (Due to cord

                compression outside the dura

                mater. Pressure on the spinal 

                cord can cause direct damage to

                neurons & also damages the 

                vessels supplying the neurons)

                - Spinal metastasis of some 

                  tumors.

                - TB spine (Caseating & 

                  granulomatous lesion affecting

                  vertebrae)

                - Primary bone tumor.

                - Intervertebral disc proalpse.

                - Extra Dural tumors.

                 

              # Intra dural extramedullary cause:

                - Intraspinal tumors like 

                  meningioma which arises from

                  meninges.

                  It causes compression of spinal                    cord.

             # Intra medullary cause: 

                - Tumors of spinal cord like 

                  Astrocytoma, Ependymoma,

                  Syringomyelia.

      

             # Miscellaneous causes:

                - Subacute combined                                        degeneration (It is a CNS                                disorder caused due to Vitamin

                  B12 deficiency. Vitamin B12 is 

                  important for synthesis of 

                  myelin sheath. Thus, impaired 

                  formation of myelin sheath 

                  leads to slowing down or 

                  stoppage of impulses)

                - Neurolathyrism (It occurs due

                  to consumption of legumes

                  which contain toxin called 

                  ODAP. This toxin causes 

                  damage to motor neuron.)

                - Arsenic poisoning (Arsenic is 

                   neurotoxic)

   

                - Fluorosis (It causes damage to

                   cytoskeleton of neurons)

                - Radiation (It causes neuronal

                    damage)

    (B) Cranial causes  :- 

        (I) Sagittal sinus thrombosis -

           Superior sagittal sinus drains blood 

           from lateral and medial surfaces of             cerebral hemispheres, including the             motor areas for both lower limbs.               Hence thrombosis in it causes                     inability to drain blood leading to                 compression and damage to these               areas resulting in Paraplegia.

 

        (II) Parasagittal Meningioma :-

           Leads to pressure over the motor                 areas for lower limbs .

    (C) Lower motor neuron causes :- 

        (I) Guillian barre syndrome :- 

          It is autoimmune disorder which 

          usually occurs after viral infection.

          The antibodies destroy myelin 

           sheath.

 

      (II) Myopathy - muscles are affected

         due to fatigue, electrolyte imbalance,

         dehydration, immune disorders, etc.

        

3) CLINICAL FEATURES OF PARAPLEGIA:-

   (a) In paraplegia due to acute causes ,

       first there is flaccidity of muscles of

       lower limb and areflexia.

       ( Flaccidity - decrease or lack of                   muscle movement due to nerve                  damage where the affected body part           becomes floppy or without muscle               tone and with diminished  reflexes.

       Areflexia - absence of deep tendon               reflexes. Tendons are the tissue that           connect muscles to bones. When you         tap on a tendon, it causes the muscle         to contract and move involuntarily.)

       # Flaccidity and areflexia occur                       initially below the level of the lesion             due to interruption of the signals                 sent via the upper motor neurons to             the lower motor neurons or related               interneurons due to damage to                     spinal cord. This period is known as

         spinal shock.

    (b) After few days or weeks , spinal 

        shock starts to resolve with                          development of spasticity and

        exaggerated tendon reflexes.

       # Reason for this -

        - There is recovery of motor neuron

          excitability.

        - There is increased denervation                      hypersensitivity .

Denervation ( i.e loss of nerve supply) leads to an initial decrease in number of neuronal membrane receptors, followed by an gradual increase in number, with enhanced sensitivity to neurotransmitters.

This leads to denervation hypersensitivity.

       - Gradual changes in muscle properties also occur following Spinal cord damage, such as fibrosis, atrophy of muscle fibers, decrease in the elastic properties, decrease in the number of sarcomeres, accumulation of connective tissue, and alteration of contractile properties.

All these anatomical changes lead to increased muscle tone which likely contribute to the increased passive tension on stretching the muscle as compared to the tension produced on stretching normal muscle.

        - This increased passive tension on stretching of affected muscle fibres leads to hyperexcitability of tonic component of stretch reflex which further results in increased muscle tone .

       

        - α-motoneurons after an UMN lesion are known to release growth factors locally . These promote local sprouting from neighbouring interneurons leading to formation of new abnormal synapses which can also contribute to spasticity.

        

        - Tendon hyper-reflexia is identified as an exaggerated muscle response to an externally applied tap of deep tendons. Reduced  inhibition of nerve fibres due to spinal cord damage is thought to play an important role in this hyper-reflexia.

        -   local sprouting of neurons in response to injury can also lead to formation of new abnormal synapses . This can also lead to abnormal reflex pathway production.

    (c) In chronic cases of paraplegia - spastic paralysis is seen because there is no sudden interruption of the signals                 sent via the upper motor neurons to             the lower motor neurons. 

Eg. Tumor compressing spinal cord - there is gradual damage to neurons. The processes of neuronal damage and production of denervation hypersensitivity are occur simultaneously i.e at one place there may be damage occuring while at the same time, production of hypersensitivity and changes in muscle properties may be occurring at other place.

    (d) There are two types of spastic paraplegia :-

(I) Paraplegia in extension :-

 increase in the extensor muscle tone leading to extension of limb.

- It occurs in initial stages of damage or when only partial damage to spinal cord has occurred.

- There may be damage to pyramidal i.e corticospinal tract.

- Extrapyramidal tracts are not damaged. Vestibulospinal tract innervates antigravity muscles i.e extensors of leg via LMN.

Thus they cause contraction of the extensors leading to extension of legs.

(II) Paraplegia in flexion :-

- flexion of limbs occur

- it occurs in the later stages of damage         when the damage progresses                       throughout the spinal cord.

- Both pyramidal and extrapyramidal              tracts may be affected.

- It may be associated with mass reflexes    (exaggerated flexor spasms).

- After an acute, complete Spinal cord            damage, flexor reflex excitability                   develops.

-Dorsal reticulospinal tract which is a part   of extrapyramidal tracts has inhibitory   control over the stretch reflex through the   activation of inhibitory circuits in the   spinal cord. It reduce the excitability of   the stretch reflex. Thus, damage to these   extrapyramidal tracts leads reduced     inhibition of flexion reflex leading to   hyperreflexia.

4) INVESTIGATIONS OF PARAPLEGIA:-

    (I) X-Ray, CT, MRI - to see lesions,                      tumor.      

    (II) CSF study - to detect infection.

5) COMPLICATIONS OF PARAPLEGIA:-

    (I) Renal infection -Most patients with spinal cord injury have urinary stasis due to neurogenic bladder, which promotes bacterial colonization. 

    (II) Renal calculi - infection of the urine by urea-splitting organisms, principally Proteus lead to formation of struvite stones.

    (III) Fecal impaction -  injury below T-12 results in damage to defecation reflex. When the bowel fills with stool the sacral nerves try to send a signal to the spinal cord to defecate but the injury disrupts the signal. 

    (IV) Pressure sore - Sitting or lying in the same position will begin to cut off the flow of blood to that area, blocking oxygen and vital nutrients from maintaining healthy tissue. When the tissue becomes starved to too long a period of time it begin to die and an pressure sore starts to form.

    (V) Contracture of limb due to                          immobilisation.

6) TREATMENT OF PARAPLEGIA:-

    (I) Treat the cause.

    (II) Bowel care :

         # Laxatives.

         # If faeces are hard -manual                           evacuation.

    (III) Bladder care :

         # Regular urinary catheterization.

         # Sometimes, urinary diversion 

            technique is needed.

         # Treatment of urinary tract infection

            & calculi, regular fluid intake.

         

    (IV) Skin care :

         # Pressure sores should be                             prevented by changing the positions

           regularly, air or water cushion.

         # If pressure sore occurs - treatment

           by antibiotics, skin grafting.

    (V) Paralysis care : 

          # Spastic paralysis may lead to

             contracture.

          # Regular passive movements 

            should be done.

          # Drugs - Baclofen (skeletal muscle

             relaxant)

          # In severe case - Intrathecal

             Baclofen in spinal canal.

    

     (VI) Rehabilitation.

      

            ⭐⭐⭐⭐⭐⭐⭐⭐⭐⭐