⭐⭐⭐ HEMIPLEGIA ⭐⭐⭐

           ⭐⭐⭐ HEMIPLEGIA ⭐⭐⭐

1) DEFINITION OF HEMIPLEGIA :-

Hemiplegia is paralysis of one side of the body.

    - Paralysis - complete or partial

    loss of muscle function leading to loss

    of ability to move.

    - Hemiplegia is caused by damage to some part( primary motor cortex) of the brain that disrupts the connection between the brain and the muscles on the affected side.

     - Primary motor cortex on the left hemisphere of the brain controls movement of the right side of the body, and right motor cortex controls movement of the left side of the body  because the nerves that travel down from the brain to the periphery cross over at the medulla (pyramid decussations) .

    - Thus, damage to the right side of the brain may cause movement problems or weakness on the body's left side and vice versa.

Above diagram helps to understand that different areas of the primary motor cortex connect to and control movement of different body parts.

       - If the area of damage is specific to only part of the primary motor cortex, such as the hand area of the homunculus, it will affect movements only of the corresponding part of their body, for example, the hand.

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2) CAUSES OF HEMIPLEGIA :-

  (A) ACUTE CAUSES :-

       (I) STROKE 

    ( Damage to the brain from interruption of its blood supply. Interruption of blood supply leads to infarction in brain.)

       - There are 2 types of strokes - ischemic stroke and hemorrhagic stroke 

       - Ischemic stroke 

 It happens when the brain's blood vessels become narrowed or blocked, causing ischemia. 

Blocked or narrowed blood vessels are caused by fatty deposits that build up in blood vessels or by blood clots 

(thrombosis or embolism ) or other substances that lodge in the blood vessels.

      - hemorrhagic stroke

  A hemorrhagic stroke is when bleeding occurs in brain which interferes with the brain's ability to function.

Reasons include:-

  # Uncontrolled high blood pressure

  # Overtreatment with anticoagulants

  # aneurysm in vessel

  # Trauma and rupture of vessel

  # Protein deposits in blood vessel walls that lead to weakness in the vessel wall (cerebral amyloid angiopathy)

  # Ischemic stroke leading to hemorrhage

  # arteriovenous malformation

      (II) TRAUMA 

(it leads to formation of hematoma by rupture of blood vessels and accumulation of blood)

          - Subdural hematoma

          - Epidural hematoma

          - Contusion

      Haematoma forms a tumour-like mass, which compresses the brain tissue and raises ICP as it expands. This increased pressure over neurons causes pressure necrosis and often results in brain injury.

       When a hemorrhage interrupts blood flow around or inside the brain, depriving it of oxygen for more than three or four minutes, the brain cells die.

(Ask about history of trauma)

      (III) OTHERS :-

          - MENINGITIS

       Meningitis causes neuronal injury by causing release of reactive oxygen intermediates, proteases, cytokines and excitatory amino acids, along with the activation of transcription factors, caspases and other proteases.

       Bacteria that enter the bloodstream and travel to the brain and spinal cord cause acute bacterial meningitis. But it can also occur when bacteria directly invade the meninges. This may be caused by an ear or sinus infection, a skull fracture, etc.

       Other symptoms of Meningitis are as follows :-

         - Fever

         - Headache

         - Impaired consciousness

         - seizures

         - Neck stiffness and rigidity

         - Photophobia

         - Vomiting

         - kernig's sign ( If patient's thigh is flexed at right angle to the abdomen and knee is tried to straighten, it doesn't straighten more than 135 degree angle.)

        - Brudzinski sign :- Patient is in supine position lying on ground. Physician's one hand is under Patient's head and other hand on patient's chest. Patient's head is lifted while applying downward pressure at chest. While doing this, patient's legs are flexed at hip and knee.

          - ENCEPHALITIS

       Nerve cells may be damaged or destroyed by both the infection( toxins) and inflammation ( release of reactive oxygen intermediates, proteases, cytokines ).

       The infection can spread through various routes like respiratory secretions or gastro-intestinal tract. Infected people colonizing the virus can spread it by sneezing, coughing and kissing or by faecal-oral route.

        

          - DRUG TOXICITY

         Following is the list of neurotoxic drugs:-

Ask for intake of any medications (drug toxicity).

          - POST SEIZURE HEMIPLEGIA

Hemiplegia and epilepsy are often related to some abnormality in the brain or an alteration in the activity of the brain. In some cases, the brain damage that causes hemiplegia may also cause epilepsy.

Neuronal injury may be induced by venous thrombosis and/or hypoxia. 

History of episodes of seizures in past should be asked.

          - MIGRAINE ASSOCIATED HEMIPLEGIA

        When some ion channel in the brain is not working properly, neurotransmitters, such as serotonin, may be released in an abnormal way. In hemiplegic migraine, some channels show dysfunction resulting in characteristic symptoms.

        There are two types of hemiplegic migraine:

      # Familial hemiplegic migraine: 

Some gene mutations cause calcium channel in nerve cells to work incorrectly  resulting in a hemiplegic migraine attack.

      # Sporadic hemiplegic migraine: In this case, there is no family history or inherited connection. The cause of SHM is unknown but probably due to new or ‘sporadic’ gene mutations.

       # History of migraine should be asked.

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    (B) SUBACUTE CAUSES :-

         (I) FAST GROWING NEOPLASMS

     - Brain tumors cause damage to neurons because they can either place pressure on normal parts of the brain causing pressure damage or spread into those areas.

     - Cancer is an electrically active tissue.  Tumor cells form synaptic connections with normal neurons that transmit electrical signals to the cancerous tissue and hence they disrupt normal synaptic circuits in brain.

The tumors also contain cell-to-cell electrical connections known as gap junctions. 

Together, the two types of connections allow electrical signals from healthy nerve cells to be conducted into and amplified within the tumors.

     - Cancer cells also express genes involved in forming synapses.

         (II) HYPOGLYCEMIA

     - Hypoglycemia causes brain fuel deprivation and, as a result, it causes damage to neurons.

( Glucose is required for ATP production and energy metabolism in neuron )

     - If abrupt energy failure occurs, the excitatory amino acid aspartate is massively released into the brain extracellular space and binds to  the excitatory amino acid receptors located on neuronal dendrites. 

Calcium fluxes occur and cell membrane breaks leading to neuronal necrosis.

       - Other neurochemical changes which are harmful for neurons include  phospholipase and other enzyme activation, tissue alkalosis, and a tendency for all cellular redox systems to shift towards oxidation.

      - Blood sugar should be checked.

         (III) PYOGENIC ABSCESS

         - It occurs when bacteria or fungi enter the brain tissue .

         - There are 3 main ways a brain abscess can develop. These are:

     # an infection in another part of the skull  such as an ear infection, sinusitis or dental abscess, which can spread directly into the brain.

     # an infection in another part of the body – for example, the infection that causes pneumonia spreading into the brain via the blood.

     # trauma, such as a severe head injury  that cracks open the skull, allowing bacteria or fungi to enter the brain.

Neuronal damage is caused by brain Infection because of bacterial toxins and  intense inflammatory response by the host (mainly neutrophils) into the CSF and subsequent neuronal death.

         (IV) GRANULOMA

Granulomas are formed as a reaction to infections, inflammation, irritants. 

Common causes include an inflammatory condition called sarcoidosis and infections such as tuberculosis. The effects of inflammation cause damage to neurons.

         (V) CEREBRAL METASTASIS in case of cancers like

Lung cancer.

Breast cancer.

Colon cancer.

Kidney cancer.

Melanoma.

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    (C) CHRONIC CAUSES :-

         (I) SLOW GROWING NEOPLASMS

     - Brain tumors cause damage to neurons because they can either place pressure on normal parts of the brain causing pressure damage or spread into those areas.

     - Cancer is an electrically active tissue. Tumor cells form synaptic connections with normal neurons that transmit electrical signals to the cancerous tissue and hence they disrupt normal synaptic circuits in brain.

The tumors also contain cell-to-cell electrical connections known as gap junctions. 

Together, the two types of connections allow electrical signals from healthy nerve cells to be conducted into and amplified within the tumors.

     - Cancer cells also express genes involved in forming synapses.

         (II) MOTOR NEURON DISEASE

         -  Motor neurons are nerve cells that send electrical output signals to the muscles, affecting the muscles' ability to function.

         - Motor neuron diseases are neurodegenerative disease which occur as the result of dysfunction of upper motor neurons in the precentral gyrus of the frontal lobe or lower motor neurons in the ventral horn of the spinal cord. In general, they cause weakness without notable sensory symptoms or pain.

       -  Pathological features of MND are loss of anterior horn cells, and of motor cells in the lower cranial nerve nuclei, and degeneration of the crossed and uncrossed corticospinal tracts.

      - Around 10% of MNDs are hereditary. The other 90% happen randomly.

      - The exact causes are unclear.  Genetic, toxic, viral, and other environmental factors may play a role.

 Inherited forms of the condition may be present at birth. They are most likely to appear after the age of 40 years.

 SMA is always hereditary, but this is not true for all forms of MND.

       -  Following may help in diagnosis :-

  Electromyography and nerve conduction studies, MRI of brain and spinal cord.

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3) CLINICAL FEATURES OF HEMIPLEGIA:-

   (I) muscle weakness or stiffness (spasticity) on one side causing trouble in walking , poor balance , trouble grabbing objects.

   (II) poor fine motor skills

   (III) Children with hemiplegia may also take longer to reach developmental milestones.

    (IV) Brain damage can also cause other symptoms such as:

          - memory problems

          - trouble concentrating

          - speech issues

          - behavior changes

          - seizures

It depends on the area affected.

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4) PATHOPHYSIOLOGY OF MUSCLE WEAKNESS AND SPASTICITY :-

   (I) Hemiplegia typically results from disruption of the corticospinal tract above the medulla. 

   (II) Tone is often increased, and posture is characterized by leg extension or slight knee flexion. Hand is also subjected to involuntary contraction of finger flexor muscles that close the hand, resulting in clenched fist and thumb-in-palm deformities.

Hemiplegic gait includes impaired natural swing at the hip and knee with leg circumduction. The pelvis is often tilted upward on the involved side to permit adequate circumduction. With ambulation, the leg moves forward and then swings back toward the midline in a circular movement. 

   (III) Hemiplegia is characterised by muscle weakness, spasticity (increased muscle tone) and sensory loss, in the arm, leg and trunk on one side of the body.

   (IV) In most cases, the upper extremity is much more affected than the lower extremity. This could be due to preference of hand usage during early development. 

   (V) Cause for spasticity 

       - Cerebrum contains the upper motor neurons (UMN). UMNs regulate the inhibitory interneurons and their effect on lower motor neurons i.e LMN. 

       - Thus, UMN may stimulate or inhibit motor actions. ( For eg :- UMNs are necessary for voluntary motor action and at the same time they exert inhibitory action on spinal cord reflex )

       - Spinal reflex activity is normally tightly regulated and if inhibitory control of UMNs over it is lost, excitation is favoured thus causing hyperexcitability of spinal reflexes. This results in characteristic spasticity. 

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5) LOCATION OF LESIONS :-

    # UPPER MOTOR NEURON type of weakness

is characterized by

  - normal muscle bulk, 

  - hypertonia (cause of spasticity is given in pathophysiology )

  - hyperreflexia,

  - clonus, 

( Clonus is involuntary and rhythmic muscle contractions that are usually initiated by a reflex.)

UMN lesion causes lack of inhibition on the tendon stretch reflex.

 Unlike small, spontaneous twitches known as fasciculations which are usually caused by lower motor neuron pathology,  clonus causes large motions that are usually initiated by a reflex.)

  - extensor plantar response (positive Babinski’s sign). 

 ( Babinski sign pathophysiology :-                     - Stimulation of the lateral plantar aspect of the foot i.e S1 dermatome normally leads to plantar flexion of the toes due to stimulation of the S1 myotome. 

     - The response results from nociceptive fibers in the S1 dermatome detecting the stimulation. Nociceptive input travels up  to the S1 region of the spine and synapse with anterior horn cells. The motor response which leads to the plantar flexion is mediated through the S1 root and tibial nerve. The toes curl down and inward. 

      - The descending fibers of the corticospinal tract i.e CST  normally prevent the ascending sensory stimulation from spreading to other nerve roots.

      -  When there is damage to the CST, nociceptive input spreads beyond S1 anterior horn cells. This leads to the L5/L4 anterior horn cells firing, which results in the contraction of toe extensors (extensor hallucis longus, extensor digitorum longus) via the deep peroneal nerve. This leads to extension (dorsiflexion or upward movement) of the big toe. Also, there may be fanning of the other toes. This is positive babinski sign.

An intact CST prevents such spread. )

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    # In cases of a LOWER MOTOR NEURON type weakness,

  - early muscle wasting, 

When alpha motor neurons die, the muscle fibers that they innervate become deprived of necessary trophic factors and eventually the muscle itself atrophies. 

  - fasciculations

Fasciculations are caused by increased receptor concentration on muscles to compensate for lack of innervation in case of LMN damage.

  - hypotonia, 

Because of the damage to alpha motor neurons and the atrophy of muscles, weakness is present in lower motor neuron disorders. 

  - hyporeflexia

  - normal plantar response.

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   (I) CORTICAL :-

     # Unequal weakness of hands & legs.

     # Seizures

 Due to decreased availability of essential substrates like glucose, oxygen.

      # Aphasia

      It occurs if dominant hemisphere is involved. The dominant hemisphere of the brain is usually the hemisphere opposite your dominant hand. ( For right-handed individuals, the dominant hemisphere is typically on the left side. )

       The dominant hemisphere of the brain controls language. In most individuals, language functions are processed in the left hemisphere. 

       Broca's area and Wernicke's area are connected by a large bundle of nerve fibres called the arcuate fasciculus. This language loop is found in the left hemisphere in about 90% of right-handed persons and 70% of left-handed persons, language being one of the functions that is performed asymmetrically in the brain.

     # Sensory deficits (damage to area having sensory function)

     # Features related to lesions in different lobes (according to the functions of respective lobes)

     # Paralysis on opposite side (due to crossing of corticospinal tract at the level of the medulla oblongata) , extent depends on area involved. 

     # No movement disorder (eg - chorea, Parkinson's, hemiballismus) because these disorders are associated with subcortical structures like basal ganglia.

     # No visual field defect [except in occipital lobe involvement. Function of occipital lobe - vision ]

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   (II) SUBCORTICAL STRUCTURES / THALAMUS :-

     # Unequal weakness of hands & legs.

     # Sensory deficits.( neurons present in the subcortical structures which carry sensory information from spinal cord to sensory cortex are damaged )

     # Paralysis on opposite side 

(due to crossing of corticospinal tract at the level of the medulla oblongata) 

     # Homonymous visual field defect

(The retina projects to four subcortical regions in the brain: 1) the lateral geniculate nucleus, the major subcortical center relaying visual information to the primary visual cortex; 

2) the superior colliculus, which control orienting eye movements;

 3) the hypothalamus, which

regulate the circadian rhythms; and 

4) the pretectum, which control the pupillary light reflex. )

     # no aphasia

     # Movement disorder

 ( chorea, parkinsonism, hemiballismus because these disorders are associated with subcortical structures like basal ganglia)

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   (III) INTERNAL CAPSULE LESIONS.

   #  hemiplegia and UMN facial palsy

Lesion extending posterior                                # Hemianesthesia

    # Homonymous hemianopia

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   (IV) BRAIN STEM LESION :-

     # Crossed or Alternating hemiplegia.

       - Alternating hemiplegia (also known as crossed hemiplegia) is a form of hemiplegia that has an ipsilateral cranial nerve palsies and contralateral hemiplegia or hemiparesis of extremities of the body.

       - The cranial nerves and cranial nerve nuclei are also located in the brainstem making them susceptible to damage from a brainstem lesion. Cranial nerves III (Oculomotor), VI (Abducens), and XII (Hypoglossal) are most often injured due to their close proximity with the pyramidal tract.

     -  Damages to these structures produce the ipsilateral presentation of paralysis or palsy due to the lack of cranial nerve decussation.

     # Features of cranial nerve damage.

(Cranial nerves originate in brainstem)

     # MID BRAIN DAMAGE :-

        -  Crossed hemiplegia - lesion in the left midbrain will result in left-sided oculomotor weakness with right hemiparesis and right facial weakness of upper motor neuron type.

       - 3rd nerve palsy

      # PONS DAMAGE :-

        - Crossed hemiplegia

A left pontine lesion will result in left facial weakness of lower motor neuron type and right-sided hemiplegia. 

       - 6th and 7th nerve palsy

      # MEDULLA DAMAGE :-

       - Crossed hemiplegia

       - 12th nerve palsy 

       - Involvement of medial lemniscus leads to loss of sensation

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   (V) SPINAL CORD :- 

      # Features of Brown Sequard Syndrome. 

( Hemiplegia on the side of damage without face involvement )

      # Effects below the level of damage :- UMN type motor and sensory loss

      # Effects at the level of damage :-

 LMN type loss.

      # Effects above the level :- hyperaesthesia.

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6) INVESTIGATIONS OF HEMIPLEGIA :-

   (I) CT scan , MRI :- haemorrhage, infarction , any swelling of the brain , meningeal enhancement, brain abscess, any tumor, granuloma, hydrocephalus.

 

   (II) Blood tests :-

       - Blood sugar ( for diabetes and hypoglycemia ), 

       - blood electrolytes

 (Hyponatremia :- In meningitis,  there is oversecretion of ADH i.e anti diuretic hormone from hypothalamus. This leads to increased water retention which dilutes the sodium levels and causes hyponatremia )

       - renal function test ( blood urea may be increased due to dehydration caused by vomiting )

       - ABGA (arterial blood gas analysis - tells about blood oxygen.) ,

       - Coagulation profile.

       - CBC (TLC is increased in Meningitis, encephalitis )

       - Blood culture (bacteremia)

   (III) Angiogram.

   (IV) Histopathology.

   (V) Checking of BP,  ECG and cardiac monitoring, neurological examination.

   (VI)  Lumbar puncture (CSF collection) :- Encephalitis, Meningitis.

   (VII) Samples of blood, urine or from the back of the throat (can be tested for viruses or other infectious agents.)

Pus culture (from ear, sinuses)

   (VIII) Electroencephalogram (EEG) :-

Certain abnormal patterns may indicate a diagnosis of encephalitis.

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7) TREATMENT OF HEMIPLEGIA :-

  (A) General Treatment :-

      # Maintainence of airway and clearance of secretions.

      # Oxygen supplementation

      # Blood electrolyte balance :- Normal saline

      # Hyperglycemia - insulin , 

          Hypoglycemia - dextrose

      # Prevent hyperthermia

      # Keep changing positions in bed - to prevent bed sores 

      # Passive movements and physiotherapy of limbs :- to prevent contractures.

      # Urinary catheterization (Foley's)

      # Nasogastric intubation (Ryle's)

      # Regular cardiac monitoring

      # Control of seizures if present.

      # Proper nutrition

  (B) Specific treatment :-

     (I) STROKE :-   

      # BP :- Urgent and sudden lowering of BP is avoided because it increases the size of infarct. Urgent lowering is indicated only in case of BP more than 220/120 mm Hg. If there is pulmonary edema, renal failure, MI or thrombolytic therapy is to be given , gradually decrease BP with antihypertensives like Labetalol, captopril, sodium nitroprusside.

      # Cerebral edema :- it occurs only in cases of large infarcts. Give mannitol, glycerol , furosemide. Dose should be monitored to prevent dehydration and electrolyte imbalance.

      # Anticoagulants - Used only in cases of mild ischemia (not in moderate and severe cases due to risk of intracerebral hemorrhage.) 

Indications :- Recent MI or other heart disease, prosthetic heart valve , thrombosis

      # Thrombolytic therapy:- 

IV recombinant Tissue plasminogen activator (rTPA) 

      Contraindications :- Bleeding disorder,

Previous neurosurgery within 3 months, Subarachnoid hemorrhage, 

BP > 185/110 mm Hg

AV malformation

   (II) INFECTION :- 

     # Antibiotics :- Ampicillin, Ceftriaxone, Cefotaxime, vancomycin, chloramphenicol

     # Steroids (they decrease complications due to host immune response ) - Dexamethasone

     # Surgery (if abscess)

   (III) TUMOR :-

     # Surgery.

     # Radiation.

  

   (IV) SUB ARACHNOID HEMORRHAGE / INTRACEREBRAL HEMORRHAGE :-

     # Surgery :- 

       - Immediate decompression of the brain to release pooled blood and relieve pressure. Decompression may be done through a burr hole procedure (drilling a hole in the skull to allow blood drainage), 

a craniectomy incision (partial removal of the skull to allow the swelling brain to expand),

 or a craniotomy (opening of the skull cavity).

         - A cerebral aneurysm that has not ruptured may require clipping through a craniotomy surgical procedure, or an angiography-type procedure to prevent a future rupture.

         - An arteriovenous malformation (AVM) that has not ruptured is treated by direct removal of the AVM through surgery, use of  radiation to close off the abnormal vessels or use of a special glue or other filler to block the blood flow from smaller blood vessels into the AVM or the vessels that supply the AVM.

       

Other treatments may include:

   # Anti-anxiety drugs 

   # medication to control blood pressure.

   # Anti-epileptic drugs for seizure control.

   #  painkillers for severe headache 

   #  stool softeners to prevent constipation and straining during bowel movements.

   (V) Stop any neurotoxic medication if present. 

 

   (VI) Treatment of conditions like sarcoidosis and infections such as tuberculosis if granuloma is present in brain.

  (VII) Motor neuron disease :-

There is no permanent cure for motor neuron disease . 

Supportive treatment is given.

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