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Neurological disorders

This document discusses neurological disorders, specifically focusing on convulsions disorders/seizure disorders/epilepsy. It defines epilepsy as recurrent episodes of cerebral origin involving disturbances of movement, sensation, behavior and consciousness. Various causes of epilepsy are described, including perinatal conditions, infections, metabolic conditions, poisoning, and genetic/hereditary syndromes. The document then classifies epilepsy and outlines the clinical features, diagnostic evaluation, and management including drug therapy, diet therapy, and surgery. Meningitis is also discussed, describing the causes, risk factors, pathophysiology, types (bacterial, viral, tuberculosis), clinical features, diagnostic evaluation, and treatment of various forms of meningitis.

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NEUROLOGICAL DISORDERS Convulsions Disorders (or) Seizure Disorders or Epilepsy It is a condition of recurrent episodes, primary of cerebral origin in which there is disturbance of movement, sensation, behaviour and consciousness. Causes:  Perinatal Condition:  Cerebral malformation  Intrauterine infection  Hypoxic- ischemic state  Trauma and haemorrhage Infection-Encephalitis:  Meningitis  Brain abscess Metabolic Condition:  Hypoglycemia, hypocalcemia, hypomag nesemia, hyponatremia, hypernatremia, storage diseases, reye syndrome, porphyria. Poisoning:  Lead, cocaine drug toxicity,  Drug with drawal Neurocutaneous Syndromes:  Tuberous sclerosis  Neurofibromatosis  Sturge-weber syndrome  Klippel-trenaumay-weber syndrome
Systemic Disorders:  Vasculitis (CNS or systemic)  SLE  Hypertensive encephalopathy  Renal failure  Hepatic encephalopathy Other:  Trauma  Tumor  Febrile  Idiopathic  Familial Classification of Epilepsy: Clinically epilepsy can be broadly classified in two groups i.e. generalized or partial 1.Generalized Seizures: 2. Tonic — &No seizures (Grand ma]) 3. Absence seizures:- i) Typical (petit ma]) ii) Atypical 4. Atopic seizures (Dropattacks) Myoclonic seizures 2. Partial Seizures: a) Simple partial seizures: (with elementary symptoms and or impaired consciousness) I. With motor signs (Jacksonians or Focal motor). II. With somato-sensory or special sensory i.c visual or auditory
III. With autonomic manifestations (Abdominal epilepsy) b) Complex partial seizures: manifested with impaired consciousness and with Automatism it include psychomotor or temporal lobe seizures. Clinical Features:  Generalized tonic-clonic seizures (grand ma! type)  The classical form has five phases, i.e an aura, tonic spasm, cionio phase and postectal phase.  Aura-dizziness tonic spasm phase-body becomes stiff, face, may become pale and distorted, eyes fixed in one position, back may be arched.  Head turned to backward in one side,  Arms are equally flexed and hands are clenched.  Due to spasm of respiratory muscles, there is ineffective breathing and cyanosis.  The clonic phase- the child may pass stool and urine involuntarily in the postectal patient become confused or exhassted or perform automatic actions  Headache 3. Absence Seizures (Petitmal): The child may loss contact with the environment for a few seconds. Day dreaming The child may discontinues the activity suddenly (e.g. reading, writing)and may resume the same activity when the seizures occur. A typical absence seizure may present as redding of the eyes, nodding of the head, slight hand movements and smacking of lips. 4. Status Epilepticus:  Cerebral damage may occur due to prolonged cerebra] hypoxia or
hypoglycemia  In postectal state the child may have cardio respiratory arrest or aspiration of vomitus. 5. Partial Seizures:  Motor, sensory, psych], or autonomic abnormalities, but consciousness is preserved 6. Myoclonic Seizures (Infantile spasms):  Cerebral abnormalities  Mental retardation  The child presents with sudden forceful myoclonic contractions involving the muscles of trunk, neck and extremities 7. Neonatal Seizures:  Eye blinking  Flutering and buccolingual movements Diagnostic Evaluation:  Careful history taking  Physical and neurological examination  Laboratory tests.  EEG:- It may confirm type of abnormality and may detect facility, extent of affection  C.T scan of head  Blood studies:-Blood glucose, calcium and lead and amino acid in serum,
to exclude metabolic causes.  Cranial imaging like x-ray of skull, PET or SPECT scan and MRI are also very useful, Parital seizure Tonic clonis simple Complex Involves both Hemispheres seizure activity Epilepsy (idiopathic/secondary) Migrane, uremia, allergies Hypoglycemic disorders, Brain damage congenital anarnalies P henylketonuri a, retarded Psychomotor development Recurrent seizure activity Pathophysiology: Non recurrent Febrile episode tumor or edema, toxins intra cranial Infection/hemorrhage, metabolic disorders Spontaneous paroxysmal electrical discharge from cortical centers Neuronal exitation in s t e m Centre cephalic (or) focal Area of the brain Spread of neuronal excitation to brain Generalized seizure Infantile spasms Absence
Jack nife Posture eyes Roll up ward Brief loss of contact with environment may have loss of consciousness Flaush, pallor or cyanosis Un conscious Involve one tonic Heriphere contractive Of muscle local motor rigidity movement related falls to To involved area of grocind Brain incontinent Sensory muscle craving r e l axat i o n Related to involved deep respiration Area of brain deep sleeps. (Numbness, haggling, Crawling sensation focal Taste in mouth) autonomic Manifestation (tachycardia Diaphoresis, blood pressure ( o r ) Papillary changes), Unfamiliarity with Events (or) environment Loss of conscious Hallucination auto matism Unusually sensation Blank start Unresponsive change in postural tone Lip smacking Drowsiness or sleep High ling
Management of epilepsy/convulsive disorders: Managements of convulsive disorders depend upon the identified course. The management mainly done with drug therapy diet therapy and surgery if indicated  Emotional support, psychosocial rehabilitation and vocational guidance are also important aspect of management.  Drug therapy:-the selection of anti epileptic drugs depends upon age type of seizure and economic status. 1. Phenobarbital-3-50 mg/kg/day in 1 or 2 divided doses and indicated in tonic-clonic partial, allmetic and febrile convulsion. 2. Diphanghy dantion -5 to 8mg/kg/day in 2 dicided doses indicated in tonic- clonic atomic, alanetic and partial seizures 3. Carbamazepine -10 to 20mg/kg/days-in 2 to 3 divided doses and indicated in tonicclonic, atonic, almetic, and partial seizures. 4. Diazepam -0.2 mg/kg/dose IV or per rectal is indicated in status eoilepsies 5. Sodium valproate -15 to 20mg/kg/day 3 to 4 divided doses in indicated has braod spectrum anticonvuisive agent. 6. Ethosuximide -10 to 20 mg/kg/day in 2 devided doses in indicated in absence seizures. Diet Therapy:  Ketogenic diet may be given to raise the seizures threshold with calculated amount of proteins and fats without carbohydrates  The child should not be given 11/ fluid with dextrose and strict fluid restriction to be maintained  Dose observation and frequent monitorining of child's conditions for vital signs airways breathing patterns preseizures events persevere of aura
etc.  Administering prescribed medications IV/IM or per rectal or oral as indicated  Following special instruction about diet and activities. Preventing Respiratory Arrest and Aspiration:  Loosen the clothing around neck and placing the child flat.  Avoid restraining the child and not to give anything in between teeth or in the mouth when the teeth are clenched during convulsions  Clear airways, remove secreations turn on, turn head one side during seizures. Promoting Socialization: Some restricted activities like, not to climb high place, or to avoid smoking and recreational activities. Strengthening Self Esteem: Promoting independence in self care and family counseling. Surgical Management:  Neurosurgery is indicated in some cases of convulsive disorders  Possible surgical interventions include corpus colostomy, focal resection of parts of cerebral cortex such as temporal lobe, extra-temporal regions involved as epileptogenic foci. Nursing Management: Nursing assessment involve subjective and objective data to be collected.
Nursing Interventions are as Follows: 1. Ensuring safety during seizures  Providepreventive measures to protect the child from injury by removal of hand objects sharp things or toys from the child.  Side rails of the bed or crib to be padded.  Removing of pharyngeal secreations by suctioning and turning head to one side  Oxygen therapy to be given and all emergency Providing Health Teaching:  Continuation of medications  Care during convulsion  Diet therapy, restricted activities, misconception regarding the disease and follow up. 2. Meningitis Infection of the central nervous system is fairly common in paediatric period. Acute bacterial meningitis, a major cause of morbidity and mortality in young children, occurs both in epidemic and sporadic pattern. Meningitis is an acute or chronic inflammation of the meningeal membrane and Cerebrospinal fluid. Incidence: Acute bacterial meningitis is common in neonate and infants than the older children.
Causes: The common organisms implicated in the neonatal Period are:  Escherichia coli  Streptococcus pneumonia  Salmonella species  Staphylococcus auras From the age of three months onwards i2-3 years the infection is due to:-  Hemophilic influenza  Streptococcus pneumonia  Meningococcal (Neisseria meningitides) Others Causes:  Septicemia  Brain and spinal cord surgeries  Pilonidal sinus  Fracture in base of skull  Inresidual with compromised immune system. Risk Factors:  Prematurity  Low birth weight  Complicated labour  Prolonged rupture of membranes  Maternal sepsis  Babies given artificial respiration
Pathogenesis: The infection casually haematogenously to meninges from the distant foci of sepsis such as pneumonia, purulent meningitis may follow head injury. Recurrent meningitis may be associated with pilonidal sinus, traumatic lesions, besides immune deficiency disorder. Classification: 1. A septic-it is due to virus 2. Septic-it is due to bacteria 3. Tuberculosis-It is caused by mycobacterium tuberculi meningitis Pathophysiology: MENINGITIS Haemophilus influenza Neissaeria meningitis (meningococcal) Streptococcus Pneumonia Over 1 month of age Nasopharyngeal Nasopharyngeal Enters cerebral blood stream from ruptured vessels From wounds, skull fracture procedure Spina bifida Inflammation of brain parenchyma Escheriachia coli Streptococcus group B Neonate
Nuchal Pia mater Arachnoid Subarachnoid space Behavioral changes Aggressiveness poor feeding Fever Head ache Neurological changes Vomiting Petechial rash Exudate thrombophlebitis Veins and venous sinuses High-pitched cry Bulging fontanellae Photophobia Confusion Seizures Stupor Nuchal rigidity Opisthotonos Coma Congestion and infarction of surrounding tissue Formation of adhesion Cranial nerve palsy Visual of auditory Impairment HydrocephalusAntibiotic therapy Maintain hydration Maintain ventilation Control seizures Resolution with or without impairment Death depending onset, type, severity, and response to therapy
1. Bacterial Meningitis: Acute bacterial meningitis is a major cause of morbidity and mortality in children. Causes:  Neisseria meningitides  Streptococcus pneumonia  Haemophilus influenza  Prolong hospital stay  Immunocompromised hosts  Post lumbar puncture or post trauma patients. Clinical Features:  Irritability, excessive crying, vomiting, head acheineck pain or stiffness in older children  Alteration in sensorium  Altered repudiation  A full anterior fontanellae  Optic disc congestion or papillederna  Seizure  Cranial nerve palsy  Focal deficit  Apanea  Cyanosis  Fever  Photophobia  Drowsiness
 Stupor  Coma  Kernigis Sign  Brudzinski sign  Clinical features of meningitis may remain masked in certain situations  Like severe protein energy malnutrition, immune compromised states malignancies,  Prolonged corticosteroid therapy etc. Diagnostic Evaluation:  History collection  Physical or neurological examination  Lumbar puncture  Cerebrospinal fluid examination  Protein  Sugar  Polymorphonucleas cells  CST pressure  CT Scan —To exclude the pressure of subdural effusion, brain abscess, hydrocephalus,  Exudates and vascular complications.  Polymerase chain reaction —To diagnose the infection with herpes simplex, entero viruses,  Meningococci and tuberculosis  Blood culture  BUN
 Serum and urine electrolyte level Treatment of Bacterial Meningitis Initial therapy should begin with third generation cephalosporin’s such as ceftriaxone or cefotxime. A combination of Ampicillin (200 mg/ kg) and chloramphenicol (100 mg/kg/24 hours) for 10-14 days.Specific Antimicrobial therapy 2. Meningococcal or Pneumococcal Meningitis: Pencillin — 4-5 lac units /kg/day 4 hourly Cefotaxime — 150-200 mg/kg/day 8 hourly Cefriaxone - 100-150 mg/kg/day 12 hourly 3. H. Influenza Meningitis: Ceftriaxone or cefotaxime —IV Alternatively, combination of ampioillin (300mg /kg/day 6 hourly)and chloramphenical (100 mg / kg/day) 4. Staphylococcal Meningitis: Vancomycin 5. Pyogenic Meningitis: Dexamethazone- 0.15 mg/kg 16 hourly for 4 days 6. Viral Meningitis: Acute Aseptic meningitis is a relatively common illness caused by a large variety factors
Clinical Features:  Fever of variable degree  Irritability  Head ache  Vomiting  Pain in neck and back  Photophobia  Sensorial loss  Nuchal rigidity  Seizures  Raised iCP  Focal deficit Diagnostic Evaluation: Lumbar puncture:  CST analysis  Blood culture  Complete blood count  Serological examination  MRT  CT scan  EEG Treatment: It include management of symptoms, fluid therapy and control of ICP Non specific therapy is available trials with
7. Tubercular Meningitis: Meningitis is a serious complication of childhood tuberculosis it is most common 4 between 6 to 12 months of age. Clinical Features: It include 3 stages 1. Predromal stage or stage of invasion 2. Stage of meningitis 3. Stage of coma 1. Predromal stage or stage of invasion:  Low grade fever loss of appetite and disturbed sleep  irritable and restless  Vomiting  Head ache  Photophobia  Constipation 2. Stage of meningitis:  Neck rigidity and kerning’s sign  Elevated temperature (390c)  Pulse slow and disturbed breathing  Increased Muscle tone  Convulsion and drowsiness  Neurological deficit like monoplegia, hemiplegia
3. Stage of coma:  Loss of consciousness and increased temperature  Altered respiration cheyne stroke respiration  Pupils are dilated and nystagmus, squint, ptosis opthalmoplegia  Bradycardia Diagnostic Evaluation:  Lumbar puncture  CSF analysis  CT scan  Serological test  X ray Complications:  Emphysema, Brain abscess, hydrocephalus  Deafness, learning difficulties, cranial nerve disorders.  Long term neurological deficits  Seizure  Increased intra craneal pressure (fCP). Treatment: a. Anti-tubercular therapy  Isoniazid -5 mg/kg/day  Rifampicin -10mg/kg/orally  Ethambutal -15-20 mg/kg/day  Pyracinamide -30mg/kg/day
b. Steroids: Parenteral corticosteroids (Dexamethasone for 1-2 weeks) c. Symptomatic Therapy: Nursing Management  Isolation  Proper hand washing  Vital signs monitored frequently  Administer medications  Bright light should be avoided  The child level of consciousness and neurologic signs are monitor  Elevate the head end.  Monitor the head circumference  When moving holding the infant and the neck should be supported  Maintain intake and out put chart and weigh the patient  Parents and their child need ongoing support during the course of illness.  Bed sore should be prevented Prognosis Prognosis related to the age of the patient. Stage at which diagnosis is made Early diagnosis and adequate and prolonged therapy improves prognosis 3 Encephalitis Encephalitis is defined as an inflammatory process of the central nervous System with dysfunction of brain.lt is an acute inflammation that is caused by viral Infection.
Causes: I. Viral a. RNA virus b. DNA virus c. Arthropod borne d. Rabies and lymphocytic choriomeningitis e. Dengue fever II. Non-viral a. Richettsia b. Fungi c. Protozoa d. Bacteria III. Post infections Typhoid, measles, mumps, Rubella, Pertusis Pathophysiology: Virus entering into the body Enter into lymphatic system Goes into blood Enter into central nervous system Antigen produce Demyelination, vascular and perivascular destruction Local vasculitic lesions with thrombus formation in brain tissue
Clinical Features:  High fever  Head ache —Vomitting  Mental confusion irritability  Apathy or loss of consciousness often associate with seizures  Sudden rise of intracranial pressure  Disturbance of speech  Neurological deficit such as ocular palsy,  hemiplegia and cerebellar syndromes ,coma  Papilledema with brain stem dysfunction  Pupillary abnormalities ,ptosis, sixth nerve palsy, opthalmoplegia  Cheyne-stoke breathing  Hyperventilation and bradycardia Diagnostic Evaluation:  History collection  Neurological examination  Lumbar puncture  CSF analysis  Polymerase chain reaction (PCR) on CSF  Stool, blood examination  ELISA  Brain biopsy  MRI  CT scan  EEG
Complications:  Temporal lobe swelling which can result in compression of the brain stem.  Aphasia, major motor and sensory deficits  Mortality and morbidity rate depend on the infectious agents, host status and other considerations. Treatment: Symptomatic and supportive therapy:  To reduce intra cranial pressure  Mannitol /IV -1g/kg as a 20 percent solution administration should be rapid. Within 20 minutes, every 4-6 hours not beyond 24- 48hours  To reduce cerebral oedema eg: Acyclovir on suspicion of herpes  For treatment on suspicion of herpes eg: Acyclovir-10mg/kg/dose Iv every 8 hourly for 10 days. Nursing Management:  Providing a quiet environment  Aspiration of nasopharyngeal secretions  Gavage or intravenous feeding  Oxygen administration  Oral hygiene  Provide skin care  catheterization and enemas  Administration of medications  Parents must be helped to understand the needed of children  Adequate nutrition provision
 Control the convulsions. 4. Hydrocephalus: The Greek term "hydrocephalus" literally meaning water logging of the head, refers to the enlargement of the head as a result of abnormally high accumulation of cerebrospinal fluid in the intracranial spaces. Incidence: Incidence of congenital hydrocephalus is not precisely known where as acquired hydrocephalus occurs 1 in 1000 children. Causes:  Excessive secretion of CSF  Abstraction of the path way of the CSF circulation eg: Inflammatory adhesions  Interfere in absorption  Thrombosis  Space occupying lesions  Intracranial infection  Neoplasm's,  Hemorrhage  Pre-exiting developmental defects Types: 1. Congenital hydrocephalus  Intracranial infection such as rubella, toxoplasmosis etc. It may cause inflammation on the lining of ventricles and meninges. This will leads to
occlusion in the pathway of CSF.  Malformation at birth a) Stenosis and mai development of the aqueduct b) Mal development of arachnoids villi c) Spinabifeda 2. Acquired hydrocephalus:  Inflammatory lesions:  Meningitis, Encephalitis.  Traumatic:  Birth trauma, head injury, intracranial hemorrhage  Neoplastic:  Space-occupying lesions like subdural hematoma or abscess.  Connective tissue disorders Pathophysiology Non communicating hydrocephalus Due to any one cause, blockage between the ventricular and subarachnoid systems Interference with the circulation of CSF Stenosis of the aqueduct of sylyius Inflammation and compression of adequate Lesions can occur in brain stem Resulting in an  Aneurysm  Subdural hemorrhage  Atresia of the foramina Obstructive hydrocephalus Communicating hydrocephalus Communication between the ventricular subarachnoid space Interference with absorption of CSF Occlusion of the subarachnoid cisterns around the brain stem May due to  Subarachnoid haemorrhage  Meningitis  Toxoplasmosis  Cytomegalo virus infection Communicating hydrocephalus Atrophy & convulsions can occur
Clinical features:  Progressive pathological enlargement of head.  Scalp becomes shiny and scalp veins will be dilated, fontanellae may be evidenced  Precession of the skull reveals typical cracked-pot sound  Sun setting phenomenon of eyes,  Lethargy.  Poor feeding  High pitched cry  Hemiplegia with steady rise in intra cranial pressure.  Hydrocephalus children's are get normal intelligence in the period of late in child hood dose not accompanying by big head.  Other feature will be presence such as  Papilloedema  Spasticity  Ataxia  Urinary incontinence  Seizures  Irritability  Headaches  Vomiting  In coordination  Confusion Diagnostic Evaluation:  X ray of skull: shows sutural separation and enlarged cranium.  MRl scan: shows Arnold chiari malformation (down ward displacement of lower
brain stem, cerebellum and fourth ventricle in to foramen magnum.  Ventriculography  Pneumoencephalography  CT Scan : used in identifying  Site of blockage  Enlargement of ventricles  Chronic subdural effusion  Cerebral atrophy Complications:  Infection  Obstruction or malfunction of shunt  Subdural hematoma  Infection or perforation of abdominal contents after placement  Death will occur if not diagnosed increased intracranial pressure. Medical management:  Administer isosorbide pre operatively  postoperatively administer acetazolamicle, frusamide, antibiotics, anticonvulsant Surgical treatment: 1. Ventriculo-peritoneal shunt (VP shunt) A ventricular catheter is inserted into the anterior portion of a lateral ventricle through a burr hole in the skull. The valve unit is tested and attached to the catheter. An incision is made in the abdomen and through the rectus muscle into the peritoneum. The end of the catheter is slipped beneath the skin of the
anterior abdominal and chest wall of the neck. After the surgery CSF flow will be normal and it is absorbed by abdominal tissues. 2. Ventriculo atrial shunt (V.A shunt) A silicone catheter is passed from dilated ventricles through burr hole and down through the internal jugular vein into the right atrium of the heart. The CSF drains into the circulating blood. Nursing management Pre operative:  Be alert to sign and symptoms that indicates  Monitor for Sign of increasing intra cranial pressure.  Record the behavior of the infant.  The infant's position is changed frequently.  Prepare the child for operation Post operative:  Monitor vital signs  Follow sterile aseptic technique  Monitor respiratory and neurostalus  Fluid restriction should be done for 24 hours  Maintain adequate hydration and nutrition  Measure intake and output carefully  Assess for signs indicating potential complication  Promote growth and development  Provide support to family and child  Observe for complication
5. Spina Bifida: Spina bifida is one of the most common congenital enamels, occurring in 1-2 /1000 live births, the defects involves spinal cord, meninges vertebra and the brain, the cones auences of the problem can affect several functions. Spina bifida is one of the most common structural congenital anomalies and imply a failure of proper closures of neural tube and mesoderm and ectoderm. Incidence: This congital anomalies occurs in about 1.5 per 1000 live births and risk in second sibling is 5 per 100 births the incidence in north India is as high 3.9-9 per 1000 live births. Classification: It is classified into meningocele and meningomyelocele. i. Spina bifida occulta Thire is no spinal cord and meninges involement. it is the mild type of spina bifida. Clinical Feature:  Tufts of hair will arise above the depressed area. ii. Meningocele: When the herniation from the vertebral column consist of meninges only and forming a CSF filled sac, the condition is called meningocele. Meningomylocele: A congenital defect of central nervous system of infants in which membranesly and the spinal cord protruded through an opening or defect in the vei/ibral
column. Pathophysiology  Maternal folic acid deficiency is an environment-factor strongly associated with neural tube defects. Serum from women with pregnancy complicated receptors and block the cellular uptake of folate. Further study is warranted to assess whether the observed association between maternal antibodies against folate receptors and neural tube defects reflects a causal relationship.  The ultimate cause of spinal dysraphism is unclear.  Dysraphic malformations probably occur when environmental agents affect underlying hereditary risk factors. Clinical Features:  The affected children usually have an anomaly of the brainstem an Arnold-chiari malformation that may result in hydrocephalus and sensory disturbances usually parallel motor dysfunction face below second lumbar vertebrae.  Flaccid, facial paralysis of lower extremities  Varying degree of sensory deficit.  Outflow incontinence with constant dribbling of urine  Defect of bowel control  Skin depression or dimple  Some seens rectal prolapse  Progressive disturbances of gait Bladder and anal sphineter paralysis. Joint deformity  Talipes vagus or yaws contrafuges Kyphosis
 Lumbosacral scoliosis  Hip dislocation Meningocele  The sac is covered only by skin and there is .np neurologic defect.  Lower body paralysis.  Bladder and bowel dysfunction  Learning disability Causes:  Exact cause unknown  Drugs  Radiation  Maternal malnutrition  Chemicals  Genetic mutation  Maternal obesity  Previous NTD pregnancy Diagnostic Evaluation:  MRI  Ultrasound  CT  Complete blood test are used primarily to determine causative organisms for the major complications mylomeninancele-meningitis
Clinical Features: Meningo myocele deficit includes varying degrees of flaccid, are flexic paraparesis and sensory deficit in the trunk and legs correspond to the inolved segments of the dysplastic cord.  Fecal and urine icontinence  Hydrocephalus may be present  impend tongue movement  Laryngeal stridor Management: Prenatal Diagnosis:-  Estimation of alpha-fetoprotien level in maternal blood between 14 and 16 weeks of gestation, or in the aminiotic fluid early pregnancy.  Ultra sound  Amniocentesis for alpha feta protein & acetyl choline esterale Diagnostic Evaluation:  Ultrasound of head and sac  CRP and X-ray of spine  Culture from lesions and draning CSF Complete blood count  Serum electrolytes and blood for cross matching Treatment Management requires a firm approach with cooperation of paediatrician, neurologist, neuro urologist and orthopedic surgeon with assistant, physiotherapist, social worker and psychiatrits.
Surgery:  It include surgery of the defect and a associated with hydrocephalus  Early closure present neurological defects  Open lesion draining CSF should be closed within 24 hours.  Closed lesion should be operated  In case, the lesion is infected, the child begin anomalies, (90%) whould die in the neonatal period. Prevention: Primary prevention folic acid supplementation to all mother including first pregnancy. Food purfication is another possible approach Counselling of family with a previous child with NTD is essential. Advise perceptional folate and offer prenatal diagnosis in subsequent pregnancy. Secondary prevention is imperative after an index care. Precaution of supplementation is 2 month, before and 3 months after conception. 6. Cerebral patsy A chronic impairment of motor control and muscle tone resulting from a non- progressive abnormality in the pyramidal motor system. It is often associated with perinatal brain ischemia, prematurity, low birth weight and birth trauma. Incidence: 1-2/1000 population. Causes: 1. From the onset of conception to the onset of labour 80 percent:  Disturbances of placental circulation,
 Cord impairment.  Intrauterine infection.  Maternal drugs or alcohol abuse,  Rh incompatibility  Post maturity  Radiation 2. During labour and delivery  Premature separation of placenta  Maternal or fetal anoxia  Premature birth  Difficult or prolonged labour.  Arrested labour progress (CPD-Cephalo  pelvic disproportion) Intracranial bleeding  Anesthetic complication  Toxemia  Precipitous delivery Use of high forceps 3. Immediate post-partum:  Hypoglycemia  Jaundice  RDS (Resp: distress syndrome)  Bleeding diathesis 4. later in childhood (incidence rate is low)  Accidental head injury  Lead poisoning
 Child abuse  Hydrocephalous  Meningitis There are three major types: 1. Spastic 2. Athertoid 3. Ataxic Clinical features:  Depend upon type  General findings includes delays and abnormalities in development especially motor control and performance  Increased or decreased muscle tone  Persistent ADD  Mental retardation  Deficits in vision or hearing Diagnostic evaluation:  Usually difficult to diagnose until child is 2-4 months or older when neurological exam reveals abnormalities  Including impairment of voluntary muscle movement and posturing Complications:  Delayed growth and development.  Skin break down.  Contractures.
 Seizures.  Difficulty with vision.  Various degree of mental retardation. Medical management:  Administer Anticonvulsant drugs and muscle relaxants eg. Diazepam, dantrolene, baclofen.  Provide physiotherapy, braces, casts, corrective appliances, glasses, hearing aids, technical aids (computer voice synthesizer) Surgery:  May necessary to correction of spastioity and contraction, tenotomy of Achilles tendon.

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Neurological disorders

  • 1.
    NEUROLOGICAL DISORDERS Convulsions Disorders(or) Seizure Disorders or Epilepsy It is a condition of recurrent episodes, primary of cerebral origin in which there is disturbance of movement, sensation, behaviour and consciousness. Causes:  Perinatal Condition:  Cerebral malformation  Intrauterine infection  Hypoxic- ischemic state  Trauma and haemorrhage Infection-Encephalitis:  Meningitis  Brain abscess Metabolic Condition:  Hypoglycemia, hypocalcemia, hypomag nesemia, hyponatremia, hypernatremia, storage diseases, reye syndrome, porphyria. Poisoning:  Lead, cocaine drug toxicity,  Drug with drawal Neurocutaneous Syndromes:  Tuberous sclerosis  Neurofibromatosis  Sturge-weber syndrome  Klippel-trenaumay-weber syndrome
  • 2.
    Systemic Disorders:  Vasculitis(CNS or systemic)  SLE  Hypertensive encephalopathy  Renal failure  Hepatic encephalopathy Other:  Trauma  Tumor  Febrile  Idiopathic  Familial Classification of Epilepsy: Clinically epilepsy can be broadly classified in two groups i.e. generalized or partial 1.Generalized Seizures: 2. Tonic — &No seizures (Grand ma]) 3. Absence seizures:- i) Typical (petit ma]) ii) Atypical 4. Atopic seizures (Dropattacks) Myoclonic seizures 2. Partial Seizures: a) Simple partial seizures: (with elementary symptoms and or impaired consciousness) I. With motor signs (Jacksonians or Focal motor). II. With somato-sensory or special sensory i.c visual or auditory
  • 3.
    III. With autonomicmanifestations (Abdominal epilepsy) b) Complex partial seizures: manifested with impaired consciousness and with Automatism it include psychomotor or temporal lobe seizures. Clinical Features:  Generalized tonic-clonic seizures (grand ma! type)  The classical form has five phases, i.e an aura, tonic spasm, cionio phase and postectal phase.  Aura-dizziness tonic spasm phase-body becomes stiff, face, may become pale and distorted, eyes fixed in one position, back may be arched.  Head turned to backward in one side,  Arms are equally flexed and hands are clenched.  Due to spasm of respiratory muscles, there is ineffective breathing and cyanosis.  The clonic phase- the child may pass stool and urine involuntarily in the postectal patient become confused or exhassted or perform automatic actions  Headache 3. Absence Seizures (Petitmal): The child may loss contact with the environment for a few seconds. Day dreaming The child may discontinues the activity suddenly (e.g. reading, writing)and may resume the same activity when the seizures occur. A typical absence seizure may present as redding of the eyes, nodding of the head, slight hand movements and smacking of lips. 4. Status Epilepticus:  Cerebral damage may occur due to prolonged cerebra] hypoxia or
  • 4.
    hypoglycemia  In postectalstate the child may have cardio respiratory arrest or aspiration of vomitus. 5. Partial Seizures:  Motor, sensory, psych], or autonomic abnormalities, but consciousness is preserved 6. Myoclonic Seizures (Infantile spasms):  Cerebral abnormalities  Mental retardation  The child presents with sudden forceful myoclonic contractions involving the muscles of trunk, neck and extremities 7. Neonatal Seizures:  Eye blinking  Flutering and buccolingual movements Diagnostic Evaluation:  Careful history taking  Physical and neurological examination  Laboratory tests.  EEG:- It may confirm type of abnormality and may detect facility, extent of affection  C.T scan of head  Blood studies:-Blood glucose, calcium and lead and amino acid in serum,
  • 5.
    to exclude metaboliccauses.  Cranial imaging like x-ray of skull, PET or SPECT scan and MRI are also very useful, Parital seizure Tonic clonis simple Complex Involves both Hemispheres seizure activity Epilepsy (idiopathic/secondary) Migrane, uremia, allergies Hypoglycemic disorders, Brain damage congenital anarnalies P henylketonuri a, retarded Psychomotor development Recurrent seizure activity Pathophysiology: Non recurrent Febrile episode tumor or edema, toxins intra cranial Infection/hemorrhage, metabolic disorders Spontaneous paroxysmal electrical discharge from cortical centers Neuronal exitation in s t e m Centre cephalic (or) focal Area of the brain Spread of neuronal excitation to brain Generalized seizure Infantile spasms Absence
  • 6.
    Jack nife Posture eyes Rollup ward Brief loss of contact with environment may have loss of consciousness Flaush, pallor or cyanosis Un conscious Involve one tonic Heriphere contractive Of muscle local motor rigidity movement related falls to To involved area of grocind Brain incontinent Sensory muscle craving r e l axat i o n Related to involved deep respiration Area of brain deep sleeps. (Numbness, haggling, Crawling sensation focal Taste in mouth) autonomic Manifestation (tachycardia Diaphoresis, blood pressure ( o r ) Papillary changes), Unfamiliarity with Events (or) environment Loss of conscious Hallucination auto matism Unusually sensation Blank start Unresponsive change in postural tone Lip smacking Drowsiness or sleep High ling
  • 7.
    Management of epilepsy/convulsivedisorders: Managements of convulsive disorders depend upon the identified course. The management mainly done with drug therapy diet therapy and surgery if indicated  Emotional support, psychosocial rehabilitation and vocational guidance are also important aspect of management.  Drug therapy:-the selection of anti epileptic drugs depends upon age type of seizure and economic status. 1. Phenobarbital-3-50 mg/kg/day in 1 or 2 divided doses and indicated in tonic-clonic partial, allmetic and febrile convulsion. 2. Diphanghy dantion -5 to 8mg/kg/day in 2 dicided doses indicated in tonic- clonic atomic, alanetic and partial seizures 3. Carbamazepine -10 to 20mg/kg/days-in 2 to 3 divided doses and indicated in tonicclonic, atonic, almetic, and partial seizures. 4. Diazepam -0.2 mg/kg/dose IV or per rectal is indicated in status eoilepsies 5. Sodium valproate -15 to 20mg/kg/day 3 to 4 divided doses in indicated has braod spectrum anticonvuisive agent. 6. Ethosuximide -10 to 20 mg/kg/day in 2 devided doses in indicated in absence seizures. Diet Therapy:  Ketogenic diet may be given to raise the seizures threshold with calculated amount of proteins and fats without carbohydrates  The child should not be given 11/ fluid with dextrose and strict fluid restriction to be maintained  Dose observation and frequent monitorining of child's conditions for vital signs airways breathing patterns preseizures events persevere of aura
  • 8.
    etc.  Administering prescribedmedications IV/IM or per rectal or oral as indicated  Following special instruction about diet and activities. Preventing Respiratory Arrest and Aspiration:  Loosen the clothing around neck and placing the child flat.  Avoid restraining the child and not to give anything in between teeth or in the mouth when the teeth are clenched during convulsions  Clear airways, remove secreations turn on, turn head one side during seizures. Promoting Socialization: Some restricted activities like, not to climb high place, or to avoid smoking and recreational activities. Strengthening Self Esteem: Promoting independence in self care and family counseling. Surgical Management:  Neurosurgery is indicated in some cases of convulsive disorders  Possible surgical interventions include corpus colostomy, focal resection of parts of cerebral cortex such as temporal lobe, extra-temporal regions involved as epileptogenic foci. Nursing Management: Nursing assessment involve subjective and objective data to be collected.
  • 9.
    Nursing Interventions areas Follows: 1. Ensuring safety during seizures  Providepreventive measures to protect the child from injury by removal of hand objects sharp things or toys from the child.  Side rails of the bed or crib to be padded.  Removing of pharyngeal secreations by suctioning and turning head to one side  Oxygen therapy to be given and all emergency Providing Health Teaching:  Continuation of medications  Care during convulsion  Diet therapy, restricted activities, misconception regarding the disease and follow up. 2. Meningitis Infection of the central nervous system is fairly common in paediatric period. Acute bacterial meningitis, a major cause of morbidity and mortality in young children, occurs both in epidemic and sporadic pattern. Meningitis is an acute or chronic inflammation of the meningeal membrane and Cerebrospinal fluid. Incidence: Acute bacterial meningitis is common in neonate and infants than the older children.
  • 10.
    Causes: The common organismsimplicated in the neonatal Period are:  Escherichia coli  Streptococcus pneumonia  Salmonella species  Staphylococcus auras From the age of three months onwards i2-3 years the infection is due to:-  Hemophilic influenza  Streptococcus pneumonia  Meningococcal (Neisseria meningitides) Others Causes:  Septicemia  Brain and spinal cord surgeries  Pilonidal sinus  Fracture in base of skull  Inresidual with compromised immune system. Risk Factors:  Prematurity  Low birth weight  Complicated labour  Prolonged rupture of membranes  Maternal sepsis  Babies given artificial respiration
  • 11.
    Pathogenesis: The infection casuallyhaematogenously to meninges from the distant foci of sepsis such as pneumonia, purulent meningitis may follow head injury. Recurrent meningitis may be associated with pilonidal sinus, traumatic lesions, besides immune deficiency disorder. Classification: 1. A septic-it is due to virus 2. Septic-it is due to bacteria 3. Tuberculosis-It is caused by mycobacterium tuberculi meningitis Pathophysiology: MENINGITIS Haemophilus influenza Neissaeria meningitis (meningococcal) Streptococcus Pneumonia Over 1 month of age Nasopharyngeal Nasopharyngeal Enters cerebral blood stream from ruptured vessels From wounds, skull fracture procedure Spina bifida Inflammation of brain parenchyma Escheriachia coli Streptococcus group B Neonate
  • 12.
    Nuchal Pia mater Arachnoid Subarachnoid space Behavioralchanges Aggressiveness poor feeding Fever Head ache Neurological changes Vomiting Petechial rash Exudate thrombophlebitis Veins and venous sinuses High-pitched cry Bulging fontanellae Photophobia Confusion Seizures Stupor Nuchal rigidity Opisthotonos Coma Congestion and infarction of surrounding tissue Formation of adhesion Cranial nerve palsy Visual of auditory Impairment HydrocephalusAntibiotic therapy Maintain hydration Maintain ventilation Control seizures Resolution with or without impairment Death depending onset, type, severity, and response to therapy
  • 13.
    1. Bacterial Meningitis: Acutebacterial meningitis is a major cause of morbidity and mortality in children. Causes:  Neisseria meningitides  Streptococcus pneumonia  Haemophilus influenza  Prolong hospital stay  Immunocompromised hosts  Post lumbar puncture or post trauma patients. Clinical Features:  Irritability, excessive crying, vomiting, head acheineck pain or stiffness in older children  Alteration in sensorium  Altered repudiation  A full anterior fontanellae  Optic disc congestion or papillederna  Seizure  Cranial nerve palsy  Focal deficit  Apanea  Cyanosis  Fever  Photophobia  Drowsiness
  • 14.
     Stupor  Coma Kernigis Sign  Brudzinski sign  Clinical features of meningitis may remain masked in certain situations  Like severe protein energy malnutrition, immune compromised states malignancies,  Prolonged corticosteroid therapy etc. Diagnostic Evaluation:  History collection  Physical or neurological examination  Lumbar puncture  Cerebrospinal fluid examination  Protein  Sugar  Polymorphonucleas cells  CST pressure  CT Scan —To exclude the pressure of subdural effusion, brain abscess, hydrocephalus,  Exudates and vascular complications.  Polymerase chain reaction —To diagnose the infection with herpes simplex, entero viruses,  Meningococci and tuberculosis  Blood culture  BUN
  • 15.
     Serum andurine electrolyte level Treatment of Bacterial Meningitis Initial therapy should begin with third generation cephalosporin’s such as ceftriaxone or cefotxime. A combination of Ampicillin (200 mg/ kg) and chloramphenicol (100 mg/kg/24 hours) for 10-14 days.Specific Antimicrobial therapy 2. Meningococcal or Pneumococcal Meningitis: Pencillin — 4-5 lac units /kg/day 4 hourly Cefotaxime — 150-200 mg/kg/day 8 hourly Cefriaxone - 100-150 mg/kg/day 12 hourly 3. H. Influenza Meningitis: Ceftriaxone or cefotaxime —IV Alternatively, combination of ampioillin (300mg /kg/day 6 hourly)and chloramphenical (100 mg / kg/day) 4. Staphylococcal Meningitis: Vancomycin 5. Pyogenic Meningitis: Dexamethazone- 0.15 mg/kg 16 hourly for 4 days 6. Viral Meningitis: Acute Aseptic meningitis is a relatively common illness caused by a large variety factors
  • 16.
    Clinical Features:  Feverof variable degree  Irritability  Head ache  Vomiting  Pain in neck and back  Photophobia  Sensorial loss  Nuchal rigidity  Seizures  Raised iCP  Focal deficit Diagnostic Evaluation: Lumbar puncture:  CST analysis  Blood culture  Complete blood count  Serological examination  MRT  CT scan  EEG Treatment: It include management of symptoms, fluid therapy and control of ICP Non specific therapy is available trials with
  • 17.
    7. Tubercular Meningitis: Meningitisis a serious complication of childhood tuberculosis it is most common 4 between 6 to 12 months of age. Clinical Features: It include 3 stages 1. Predromal stage or stage of invasion 2. Stage of meningitis 3. Stage of coma 1. Predromal stage or stage of invasion:  Low grade fever loss of appetite and disturbed sleep  irritable and restless  Vomiting  Head ache  Photophobia  Constipation 2. Stage of meningitis:  Neck rigidity and kerning’s sign  Elevated temperature (390c)  Pulse slow and disturbed breathing  Increased Muscle tone  Convulsion and drowsiness  Neurological deficit like monoplegia, hemiplegia
  • 18.
    3. Stage ofcoma:  Loss of consciousness and increased temperature  Altered respiration cheyne stroke respiration  Pupils are dilated and nystagmus, squint, ptosis opthalmoplegia  Bradycardia Diagnostic Evaluation:  Lumbar puncture  CSF analysis  CT scan  Serological test  X ray Complications:  Emphysema, Brain abscess, hydrocephalus  Deafness, learning difficulties, cranial nerve disorders.  Long term neurological deficits  Seizure  Increased intra craneal pressure (fCP). Treatment: a. Anti-tubercular therapy  Isoniazid -5 mg/kg/day  Rifampicin -10mg/kg/orally  Ethambutal -15-20 mg/kg/day  Pyracinamide -30mg/kg/day
  • 19.
    b. Steroids: Parenteral corticosteroids(Dexamethasone for 1-2 weeks) c. Symptomatic Therapy: Nursing Management  Isolation  Proper hand washing  Vital signs monitored frequently  Administer medications  Bright light should be avoided  The child level of consciousness and neurologic signs are monitor  Elevate the head end.  Monitor the head circumference  When moving holding the infant and the neck should be supported  Maintain intake and out put chart and weigh the patient  Parents and their child need ongoing support during the course of illness.  Bed sore should be prevented Prognosis Prognosis related to the age of the patient. Stage at which diagnosis is made Early diagnosis and adequate and prolonged therapy improves prognosis 3 Encephalitis Encephalitis is defined as an inflammatory process of the central nervous System with dysfunction of brain.lt is an acute inflammation that is caused by viral Infection.
  • 20.
    Causes: I. Viral a. RNAvirus b. DNA virus c. Arthropod borne d. Rabies and lymphocytic choriomeningitis e. Dengue fever II. Non-viral a. Richettsia b. Fungi c. Protozoa d. Bacteria III. Post infections Typhoid, measles, mumps, Rubella, Pertusis Pathophysiology: Virus entering into the body Enter into lymphatic system Goes into blood Enter into central nervous system Antigen produce Demyelination, vascular and perivascular destruction Local vasculitic lesions with thrombus formation in brain tissue
  • 21.
    Clinical Features:  Highfever  Head ache —Vomitting  Mental confusion irritability  Apathy or loss of consciousness often associate with seizures  Sudden rise of intracranial pressure  Disturbance of speech  Neurological deficit such as ocular palsy,  hemiplegia and cerebellar syndromes ,coma  Papilledema with brain stem dysfunction  Pupillary abnormalities ,ptosis, sixth nerve palsy, opthalmoplegia  Cheyne-stoke breathing  Hyperventilation and bradycardia Diagnostic Evaluation:  History collection  Neurological examination  Lumbar puncture  CSF analysis  Polymerase chain reaction (PCR) on CSF  Stool, blood examination  ELISA  Brain biopsy  MRI  CT scan  EEG
  • 22.
    Complications:  Temporal lobeswelling which can result in compression of the brain stem.  Aphasia, major motor and sensory deficits  Mortality and morbidity rate depend on the infectious agents, host status and other considerations. Treatment: Symptomatic and supportive therapy:  To reduce intra cranial pressure  Mannitol /IV -1g/kg as a 20 percent solution administration should be rapid. Within 20 minutes, every 4-6 hours not beyond 24- 48hours  To reduce cerebral oedema eg: Acyclovir on suspicion of herpes  For treatment on suspicion of herpes eg: Acyclovir-10mg/kg/dose Iv every 8 hourly for 10 days. Nursing Management:  Providing a quiet environment  Aspiration of nasopharyngeal secretions  Gavage or intravenous feeding  Oxygen administration  Oral hygiene  Provide skin care  catheterization and enemas  Administration of medications  Parents must be helped to understand the needed of children  Adequate nutrition provision
  • 23.
     Control theconvulsions. 4. Hydrocephalus: The Greek term "hydrocephalus" literally meaning water logging of the head, refers to the enlargement of the head as a result of abnormally high accumulation of cerebrospinal fluid in the intracranial spaces. Incidence: Incidence of congenital hydrocephalus is not precisely known where as acquired hydrocephalus occurs 1 in 1000 children. Causes:  Excessive secretion of CSF  Abstraction of the path way of the CSF circulation eg: Inflammatory adhesions  Interfere in absorption  Thrombosis  Space occupying lesions  Intracranial infection  Neoplasm's,  Hemorrhage  Pre-exiting developmental defects Types: 1. Congenital hydrocephalus  Intracranial infection such as rubella, toxoplasmosis etc. It may cause inflammation on the lining of ventricles and meninges. This will leads to
  • 24.
    occlusion in thepathway of CSF.  Malformation at birth a) Stenosis and mai development of the aqueduct b) Mal development of arachnoids villi c) Spinabifeda 2. Acquired hydrocephalus:  Inflammatory lesions:  Meningitis, Encephalitis.  Traumatic:  Birth trauma, head injury, intracranial hemorrhage  Neoplastic:  Space-occupying lesions like subdural hematoma or abscess.  Connective tissue disorders Pathophysiology Non communicating hydrocephalus Due to any one cause, blockage between the ventricular and subarachnoid systems Interference with the circulation of CSF Stenosis of the aqueduct of sylyius Inflammation and compression of adequate Lesions can occur in brain stem Resulting in an  Aneurysm  Subdural hemorrhage  Atresia of the foramina Obstructive hydrocephalus Communicating hydrocephalus Communication between the ventricular subarachnoid space Interference with absorption of CSF Occlusion of the subarachnoid cisterns around the brain stem May due to  Subarachnoid haemorrhage  Meningitis  Toxoplasmosis  Cytomegalo virus infection Communicating hydrocephalus Atrophy & convulsions can occur
  • 25.
    Clinical features:  Progressivepathological enlargement of head.  Scalp becomes shiny and scalp veins will be dilated, fontanellae may be evidenced  Precession of the skull reveals typical cracked-pot sound  Sun setting phenomenon of eyes,  Lethargy.  Poor feeding  High pitched cry  Hemiplegia with steady rise in intra cranial pressure.  Hydrocephalus children's are get normal intelligence in the period of late in child hood dose not accompanying by big head.  Other feature will be presence such as  Papilloedema  Spasticity  Ataxia  Urinary incontinence  Seizures  Irritability  Headaches  Vomiting  In coordination  Confusion Diagnostic Evaluation:  X ray of skull: shows sutural separation and enlarged cranium.  MRl scan: shows Arnold chiari malformation (down ward displacement of lower
  • 26.
    brain stem, cerebellumand fourth ventricle in to foramen magnum.  Ventriculography  Pneumoencephalography  CT Scan : used in identifying  Site of blockage  Enlargement of ventricles  Chronic subdural effusion  Cerebral atrophy Complications:  Infection  Obstruction or malfunction of shunt  Subdural hematoma  Infection or perforation of abdominal contents after placement  Death will occur if not diagnosed increased intracranial pressure. Medical management:  Administer isosorbide pre operatively  postoperatively administer acetazolamicle, frusamide, antibiotics, anticonvulsant Surgical treatment: 1. Ventriculo-peritoneal shunt (VP shunt) A ventricular catheter is inserted into the anterior portion of a lateral ventricle through a burr hole in the skull. The valve unit is tested and attached to the catheter. An incision is made in the abdomen and through the rectus muscle into the peritoneum. The end of the catheter is slipped beneath the skin of the
  • 27.
    anterior abdominal andchest wall of the neck. After the surgery CSF flow will be normal and it is absorbed by abdominal tissues. 2. Ventriculo atrial shunt (V.A shunt) A silicone catheter is passed from dilated ventricles through burr hole and down through the internal jugular vein into the right atrium of the heart. The CSF drains into the circulating blood. Nursing management Pre operative:  Be alert to sign and symptoms that indicates  Monitor for Sign of increasing intra cranial pressure.  Record the behavior of the infant.  The infant's position is changed frequently.  Prepare the child for operation Post operative:  Monitor vital signs  Follow sterile aseptic technique  Monitor respiratory and neurostalus  Fluid restriction should be done for 24 hours  Maintain adequate hydration and nutrition  Measure intake and output carefully  Assess for signs indicating potential complication  Promote growth and development  Provide support to family and child  Observe for complication
  • 28.
    5. Spina Bifida: Spinabifida is one of the most common congenital enamels, occurring in 1-2 /1000 live births, the defects involves spinal cord, meninges vertebra and the brain, the cones auences of the problem can affect several functions. Spina bifida is one of the most common structural congenital anomalies and imply a failure of proper closures of neural tube and mesoderm and ectoderm. Incidence: This congital anomalies occurs in about 1.5 per 1000 live births and risk in second sibling is 5 per 100 births the incidence in north India is as high 3.9-9 per 1000 live births. Classification: It is classified into meningocele and meningomyelocele. i. Spina bifida occulta Thire is no spinal cord and meninges involement. it is the mild type of spina bifida. Clinical Feature:  Tufts of hair will arise above the depressed area. ii. Meningocele: When the herniation from the vertebral column consist of meninges only and forming a CSF filled sac, the condition is called meningocele. Meningomylocele: A congenital defect of central nervous system of infants in which membranesly and the spinal cord protruded through an opening or defect in the vei/ibral
  • 29.
    column. Pathophysiology  Maternal folicacid deficiency is an environment-factor strongly associated with neural tube defects. Serum from women with pregnancy complicated receptors and block the cellular uptake of folate. Further study is warranted to assess whether the observed association between maternal antibodies against folate receptors and neural tube defects reflects a causal relationship.  The ultimate cause of spinal dysraphism is unclear.  Dysraphic malformations probably occur when environmental agents affect underlying hereditary risk factors. Clinical Features:  The affected children usually have an anomaly of the brainstem an Arnold-chiari malformation that may result in hydrocephalus and sensory disturbances usually parallel motor dysfunction face below second lumbar vertebrae.  Flaccid, facial paralysis of lower extremities  Varying degree of sensory deficit.  Outflow incontinence with constant dribbling of urine  Defect of bowel control  Skin depression or dimple  Some seens rectal prolapse  Progressive disturbances of gait Bladder and anal sphineter paralysis. Joint deformity  Talipes vagus or yaws contrafuges Kyphosis
  • 30.
     Lumbosacral scoliosis Hip dislocation Meningocele  The sac is covered only by skin and there is .np neurologic defect.  Lower body paralysis.  Bladder and bowel dysfunction  Learning disability Causes:  Exact cause unknown  Drugs  Radiation  Maternal malnutrition  Chemicals  Genetic mutation  Maternal obesity  Previous NTD pregnancy Diagnostic Evaluation:  MRI  Ultrasound  CT  Complete blood test are used primarily to determine causative organisms for the major complications mylomeninancele-meningitis
  • 31.
    Clinical Features: Meningo myoceledeficit includes varying degrees of flaccid, are flexic paraparesis and sensory deficit in the trunk and legs correspond to the inolved segments of the dysplastic cord.  Fecal and urine icontinence  Hydrocephalus may be present  impend tongue movement  Laryngeal stridor Management: Prenatal Diagnosis:-  Estimation of alpha-fetoprotien level in maternal blood between 14 and 16 weeks of gestation, or in the aminiotic fluid early pregnancy.  Ultra sound  Amniocentesis for alpha feta protein & acetyl choline esterale Diagnostic Evaluation:  Ultrasound of head and sac  CRP and X-ray of spine  Culture from lesions and draning CSF Complete blood count  Serum electrolytes and blood for cross matching Treatment Management requires a firm approach with cooperation of paediatrician, neurologist, neuro urologist and orthopedic surgeon with assistant, physiotherapist, social worker and psychiatrits.
  • 32.
    Surgery:  It includesurgery of the defect and a associated with hydrocephalus  Early closure present neurological defects  Open lesion draining CSF should be closed within 24 hours.  Closed lesion should be operated  In case, the lesion is infected, the child begin anomalies, (90%) whould die in the neonatal period. Prevention: Primary prevention folic acid supplementation to all mother including first pregnancy. Food purfication is another possible approach Counselling of family with a previous child with NTD is essential. Advise perceptional folate and offer prenatal diagnosis in subsequent pregnancy. Secondary prevention is imperative after an index care. Precaution of supplementation is 2 month, before and 3 months after conception. 6. Cerebral patsy A chronic impairment of motor control and muscle tone resulting from a non- progressive abnormality in the pyramidal motor system. It is often associated with perinatal brain ischemia, prematurity, low birth weight and birth trauma. Incidence: 1-2/1000 population. Causes: 1. From the onset of conception to the onset of labour 80 percent:  Disturbances of placental circulation,
  • 33.
     Cord impairment. Intrauterine infection.  Maternal drugs or alcohol abuse,  Rh incompatibility  Post maturity  Radiation 2. During labour and delivery  Premature separation of placenta  Maternal or fetal anoxia  Premature birth  Difficult or prolonged labour.  Arrested labour progress (CPD-Cephalo  pelvic disproportion) Intracranial bleeding  Anesthetic complication  Toxemia  Precipitous delivery Use of high forceps 3. Immediate post-partum:  Hypoglycemia  Jaundice  RDS (Resp: distress syndrome)  Bleeding diathesis 4. later in childhood (incidence rate is low)  Accidental head injury  Lead poisoning
  • 34.
     Child abuse Hydrocephalous  Meningitis There are three major types: 1. Spastic 2. Athertoid 3. Ataxic Clinical features:  Depend upon type  General findings includes delays and abnormalities in development especially motor control and performance  Increased or decreased muscle tone  Persistent ADD  Mental retardation  Deficits in vision or hearing Diagnostic evaluation:  Usually difficult to diagnose until child is 2-4 months or older when neurological exam reveals abnormalities  Including impairment of voluntary muscle movement and posturing Complications:  Delayed growth and development.  Skin break down.  Contractures.
  • 35.
     Seizures.  Difficultywith vision.  Various degree of mental retardation. Medical management:  Administer Anticonvulsant drugs and muscle relaxants eg. Diazepam, dantrolene, baclofen.  Provide physiotherapy, braces, casts, corrective appliances, glasses, hearing aids, technical aids (computer voice synthesizer) Surgery:  May necessary to correction of spastioity and contraction, tenotomy of Achilles tendon.