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Spastic Quadriparesis: Etiology, Clinical Features, and Multimodal Management

Spastic quadriparesis (tetraparesis) denotes weakness and spasticity in all four limbs resulting from upper motor neuron (UMN) damage. It is a clinical syndrome, not a specific disease.

Major Etiologies

Category	Conditions
Perinatal	Cerebral palsy (spastic quadriplegic type), hypoxic-ischemic encephalopathy
Acquired brain	Traumatic brain injury, stroke (bilateral hemispheric/brainstem), encephalitis
Demyelinating	Multiple sclerosis, ADEM, NMOSD
Spinal cord	Cervical spondylotic myelopathy, trauma, tumor, transverse myelitis
Degenerative	ALS (UMN predominant), HSP, spinocerebellar ataxias
Metabolic/Genetic	Leukodystrophies, mitochondrial disorders

Clinical Features

Spasticity: Velocity-dependent increase in tone (clasp-knife), hyperreflexia, clonus, Babinski sign.
Weakness: Pyramidal distribution (extensors > flexors upper extremities; flexors > extensors lower extremities).
Motor control: Impaired dexterity, gait (scissoring, circumduction), balance.
Associated: Dysarthria, dysphagia, pseudobulbar affect, cognitive impairment, epilepsy.

Management Framework

Tone reduction: Oral baclofen, tizanidine, diazepam; intrathecal baclofen pump (severe); BoNT-A/B injections (focal).
Rehabilitation: PT (stretching, strengthening, gait training), OT (ADLs, splinting), SLP (swallowing, communication).
Orthopedic: Tendon releases, osteotomies, spinal fusion (scoliosis).
Assistive technology: Power wheelchairs, AAC devices, environmental control systems.
Disease-modifying: DMTs for MS; specific metabolic/genetic therapies.
Palliative/supportive: Respiratory care, nutrition, skin integrity, psychosocial support.

Prognosis

Varies by etiology: static (cerebral palsy) vs. progressive (MS, ALS, HSP). Early, intensive, interdisciplinary care maximizes function and quality of life across the lifespan.

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