Bronchial Asthma 1 Lung and Pleura Asthma is a common disease and defined as chronic inflammatory disorder of the airways. ESSENTIALS OF DIAGNOSIS Clinical Investigation Episodic or chronic symptoms of airways obstruction: Pulmonary function tests: (T able 1.1) Breathlessness Limitation of airflow Cough Positive bronchial provocation challenge Wheezing Complete or partial reversibility of airflow Chest tightness obstruction, either spontaneously or Prolonged expiration, dif fuse wheezing and follow ing bronchodilatation therapy rhonchi on physical examination Table 1.1: Pulmonary function test in bronchial asthma Spir ometry : I. a. FEV 1 (Forced expiratory volume in the first second) b . FVC (Forced vital capacity) Fall in the ratio of FEV1 to FVC points to airway obstruction due to asthma, COPD, bronchiectasis and upper airway obstruction I I . Spirometry repeated after use of bronchodilators. In asthma relief is obtained MANAGEMENT Antiasthmatic Drugs Classification: I. Long-term medications: 1. Corticosteroids: a . Inhaled corticosteroid: Beclomethasone dipropion ate Budesonide Fluticasone T riamcinolone, acetonide b . Systemic corticosteroids: Prednisolone tablet Methylprednisolone tablet 2. Cromolyn inhaler 3. Long acting B2 agonists: Salmeterol inhaler Salmeterol sustained release tablet 4 . Theophylline tablet 5.

Lung Abscess 2 L ung and Pleura PREVENTION 1 . Measures to reduce aspiration. 2 . Early treatment of pneumonia. 3 . Adequate use of antibiotics to reduce relapse. 4 . Adequate care of periodontal disease. MEDICAL MANAGEMENT A. Antibiotic therapy: Flow chart: Determine whether infection is community acquired or hospital acquired. Community acquir e d Hospital acquir e d a . Penicillin 5 to 40 million units/day till Usually mixed infection with Klebsiella, Pseudo - defervescence (in 3-6 weeks), followed by monas , S taphylococcus aur eus : oral penicillin G , V , ampicillin in dosages 3rd generation cephalosporin of 500 to 750 mg 4 hourly + In case of penicillin resistance: Clindamycin Gentamicin 600 mg IV every 6 to 8 hours until patient is + afebrile, followed by clindamycin 300 mg Metronidazole for 6 to 8 weeks 4 times a day orally or b . Alternatively: Penicillin 10-20 million units/day IV + Metronidazole 2 gm orally/day in 2-4 divided dosages B. T r eatment of causes of lung abscess: Antibiotics according to culture and sensitivity Aspiration of infected material specially in unconscious patients, alcohol abuse, sedatives, CV A , head injury and dysphagia (due to achalasia, oesophageal stricture or bulbar palsy). C. Physiotherapy a . Postural drainage b .

Bronchiectasis 3 L ung and Pleura PREVENTION Prevention depends upon treatable precipitating causes: Pr ecipitating factors Pr evention 1. Foreign body inhalation aspiration of Early and adequate management gastric content 2 . Empyema Do 3. Childhood respiratory infection Prompt treatment (pneumonia, bronchopneumonia, whooping cough) 4. Sinus infection Do Infection of oral cavity 5. Recurrent infection Influenzal vaccine MEDICAL MANAGEMENT A . Management of bronchial secretion: a . Postural drainage b. Expectorants such as potassium iodide. They are of questionable value. c . Mucolytic agents such as bromhexine. d. Bronchodilators for bronchospasm. e . Regular physical therapy . B. Antibiotics for infection (characterised by cough, blood streaked sputum, purulent sputum, progressive dyspnoea and weight loss): a . Usual antibiotics: Ampicillin, cephalosporin, tetracycline, chloramphenicol, cotrimoxazole. T etracycline, chloramphenicol and cotrimoxazole given if patient is aller gic to penicillin. b. For anaerobes producing foul-smelling sputum: Metronidazole. c . Remember culture may be sterile. Duration of antibiotic therapy: Usually 1-3 weeks or after sputum becomes less purulent. In cystic fibrosis long-term course of antibiotics is needed. C . General: a . Attention to general health and nutrition is essential. b. Hydration is ef fective like expectorants. c . Cessation of smoking. D . Oxygen for hypoxia during acute exacerbation.

Diffuse Interstitial Lung Disease 4 L ung and Pleura CLASSIFICATION There are hundreds of causes of interstitial lung disease (ILD) but only clinically important diseases are mentioned in the following table: Table 4.1: Causes of interstitial lung disease (ILD) I. Idiopathic pulmonary fibrosis (cryptogenic fibrosing alveolitis) I I . Disorders associated with ILD: 1 . ILD associated with collagen vascular disorders: Rheumatoid arthritis Systemic lupus erythromatosus (SLE) Progressive systemic sclerosis Polymyositis 2 . Occupational lung diseases: (pneumoconiosis) Silicosis Asbestosis Siderosis Berylliosis T alcosis 3 . ILD associated with pulmonary vascular diseases: W egner s granulomatosus Goodpasture s syndrome Pulmonary vasculitis 4 . Inherited disorders: Familial idiopathic pulmonary fibrosis Neurofibromatosis T uberous sclerosis Neimann-Pick disease Gaucher s disease 5 . Infection: Miliary tuberculosis Disseminated histoplasmosis Pneumocystis carinii pneumonia 6 . Physical and chemical agents: Radiation injury Inhalation of toxic gases contd...

Pulmonary Thromboembolism (PTE) 5 Lung and Pleura DIAGNOSTIC APPROACH It includes two parts: A . Diagnosis of deep vein thrombosis in legs. B . Diagnosis of pulmonary thromboembolism. Diagnosis of D eep Vein T hrombosis (DVT) In 95% cases PTE is complication of DVT of lower extremities: i . Look for predisposing factors of DVT : Hip fracture, recent major sur gery , past history of thrombophlebitis, bedrest for more than a few days in medical conditions such a CCF , acute myocardial infarction, pregnancy , pelvic disease, malignancy , oral contraceptives. ii. Look for signs: Local pain, redness, heat and oedema in legs. iii. Investigate for DVT Doppler studies Impedence plethysmography  T oo subjective Best choice Non-investive, safe and easily hence not very available specific Normal: Abnormal: a . Rules out DVT in Confirms DVT 95% cases b.

Pulmonary Atelectasis and Fibrosis 6 L ung and Pleura PULMONARY ATELECTASIS For treatment purpose causes of atelectasis must be known for rational therapy . Causes are summarised below: Congenital causes Premature birth, neonatal hyaline membrane disease. Acquired causes A . Compression collapse due to external compression by pleural ef fusion, haemothorax, pneumothorax, enlar ged gland and aortic aneurysm. B . Absorption collapse due to bronchial obstruction: Intraluminal causes: Bronchial wall causes: Foreign body , Bronchial stricture often due to TB and tumour inspissated mucus, tumour and aspiration of gastric content during anaesthesia or in comatosed state Diagnostic C lues Clinical M anifestations A . Slowly developing atelectasis: Asymptomatic B . Acute, sudden and rapidly developing atelectasis: Cough, dyspnoea. Usually occurs in obstructive collapse due to FB or during operation. C . Massive collapse: Cynosis, restlessness, tachycardia, occasionally circulatory collapse. Signs on affected side Limited chest excursion, shift of trachea and heart to the same side, resonance diminished, breath sound and vocal resonance markedly diminished, bronchial breathing, whispering pectoriloquy and acute respiratory failure in massive collapse. Investigations A . X-ray chest: Shrunken lung, lobe or segment, displaced fissures, elevated diaphragm and mediastinal shift.

Treatment for Eosinophilic Diseases of Lungs 7 L ung and Pleura DOSAGES AND INDICATIONS Corticosteroids 1. Simple pulmonary eosinophilia (Loeffler s syndr ome): Resolves spontaneously in one month. Prednisolone rarely required. 2. Chr onic eosinophilic pneumonia: Prednisolone 30-40 mg/dayreduces symptoms within 24- 48 hours. If corticosteroids are discontinued in the first 6 months, relapse may occur . Most patients do not relapse after 6 months treatment. 3. Acute eosinophilic pneumonia: Methylprednisolone 60-125 mg every 6 hour until respiratory failure resolves usually within 1-3 days and then 40-60 mg per day for 2-4 weeks and then tapered over the next 2-4 weeks. 4. Idiopathic hyper eosinophilic syndr ome: Prednisolone 60 mg/day for a week, and then 60 mg every other day for 3 months. Fifty per cent show good response. 5. T r opical pulmonar y eosinophilia: S teroids significantly reduces the lower respiratory tract inflammation. 6. D rug induced pulmonary eosinophilia: W ithdraw the drug. In severe and persistent cases need short course of steroids. Diethylcarbamazine (DEC) T r opical pulmonar y eosinophilia: DEC 6-12 mg/kg body weight/day . Relapse occurs even with steroids in 20% cases and hence repeat monthly course of DEC at 2-3 monthly intervals for a period of 1-2 years. Cytotoxic D rugs Busulfan, hydroxyurea, cyclophosphamide, interferon, cyclosporine-A etoposide and vincristine. They are used in idiopathic hypereosinophilic syndrome and Langerhan s cell granuloma of the lung. Radiation T herapy Langerhan s cell granulomatosis : Granulomatosus masses compressing the chest wall and adjacent lung may resolve with radiation therapy .

Treatment of Sarcoidosis 8 L ung and Pleura TREATMENT OF SARCOIDOSIS It is essentially symptomatic. I. Corticoster oids Indications Dosages and pr eparations Remarks and pr ognosis a . Depends upon clinical, Prednisolone : Start a . In W est, remission rate radiological and functional 0.5-1 mg/kg body wt 80-90% and may last for findings.  lifetime. In India, relapses b. Absolute indications: Gradually tapered to 10-15 mg are common. i. Involvement of CNS, eye, /day in 3-6 months and conti- b. Severe cases do not remit. heart or any other vital nued for a year or two c . T erminal complications o r gans  are respiratory failure, ii. Acute symptoms with hyper- Followed carefully , if signs renal failure, cardiac calcaemia and breathlessness of recurrence observed, failure, corpulmonale or with hypoxaemia treatment started again. massive haemoptysis. II. Patients who contact tuber culosis : If tuberculin test is positive, prophylactic and curative treatment should be given. III. Ophthalmic and skin lesions : T opical steroids, chloroquine, methotrexate. IV . Ar thritis occurring in Loefgr en s syndr ome : Indomethacin, NSAID. V. Hyper calcaemia and hyper calciuria : S top milk and cheese, avoid sun bathing, stop vitamin D.  If fails  start corticosteroids VI. Other drugs : 1. Chloroquine: Have some suppressive effect on labile sarcoid infiltration of lung and skin. Dose: 200 mg twice daily . Should not be continued for more than 6 months. 2. Cytotoxic and immunosuppressive drugs. They have suppressive ef fect on sarcoid granuloma resistant to steroids.

Bronchogenic Carcinoma 9 L ung and Pleura TREATMENT T reatment depends on a number of factors: T ype of lung cancer (non-small or small cell lung cancer) Size of tumour Location of tumour Extent of tumour General health of patient Aim is to control lung cancer , and/or improve quality-of-life by reducing symptoms. Table 9.1: Types of treatment, indications, procedures and prognosis T ypes of tr eatment Indications P r ocedur es P r ognosis Sur ger y Chemotherapy Kill cancer cells throughout the body . Controls cancer growth and relieves symptoms Radiation therapy High ener gy rays kill cancer cells Non-small cell type and stage I and II Some tumours are inoperable because of size and location or for other medical reasons a . Locally advanced sur g i - cally resectable disease b . Malignant pleural ef fusion c . Superior mediastinal com- pression syndrome a . T reatment of choice in patients who are unfit for operation. b . Used before sur gery to shrink tumour , or after sur gery to destroy any cancer cells that remain in the treated area. Resection of primary tumour and regional lymph nodes: a . W edge resection: Only a small part or segment of lung removed. b . Lobectomy: Whole lobe removed. c . Pneumonectomy: Remo- val of entire lung. a . Most drugs given by injec- tion directly into vein. b . Or by catheter into vein. c . Some drugs given in the form of a pill. Drugs used: Cisplatin, carboplatin, ifosamide, vinidestine, vinblastine, etopo- side, mitomycin C. T wo types of radiation therapy : a . External radiation from a machine b . Internal radiation comes from an implant (a small container of radioactive material) placed directly into or near the tumour . Only 30-35% operated patients survive for 5 years, giving overall survival rate of 4%. a . Radiation + chemotherapy increases survival rate. b. Radiation is as good as sur gery in slowly growing epidermoid carcinoma. contd...

Pneumonia 10 L ung and Pleura PREVENTION Prevention usually revolves round the precipitating factors for pneumonia: Pr ecipitating factors Pr evention Immunosuppression (diabetes, HIV infection, Pneumococcal vaccine immunosuppressive drugs Coexisting disease such as pulmonary , cardiac, Pneumococcal vaccine renal and liver diseases IV drugs abuse Pneumococcal vaccine Aspiration of oropharyngeal contents Head up position (30 degree) during nasogastric (unconscious patients, oesophageal obstruction tube feeding, prevention feeding tube dislodgement, suction, frequent position change, chest physio- therapy . Removal of nasogastric and endotracheal tubes early . Alcohol, smoking Discontinuance of smoking and alcohol. Mechanical ventilation Disinfection of respiratory equipment should be done between patients and change of respiratory tube every 48 hours. Cleaning and drying nebulisers. Legionellosis pneumonia precipitated by T u rning off the equipments. a . Contaminated cooling towers, airconditio- ners, evaporative condensers, humidifiers b. Potable water Raising the temperature of hot water to above 55 degree C or by hyperchlorination ANTIBIOTIC THERAPY Antibiotic therapy is based on or ganisms involved and types of pneumonia. (T able 10.1) Table 10.1: Types and organisms of pneumonia I. Primary pneumonia (community acquired) O r ganisms : S. pneumoniae, S. aur eus, M. pneumoniae , Legionellosis pneumoniae , H. influenzae , Klebsiella, S. pyogenes, Coxiella, Chlamydia, Actinomyces, V iruses (measles, varicella, cytomegalovirus) contd...

Treatment of Viral Respiratory Infection Mycoplasma Pneumoniae and Legionellosis 11 L ung and Pleura Diseases Symptomatic tr eatment Specific tr eatment P r evention Treatment of Viral Respiratory Infection Mycoplasma Pneumoniae and Legionellosis Table 11.1: Diseases, symptomatic treatment, specific treatment and prevention V iral upper respiratory tract infection Respiratory syncytial virus Influenzal virus a. Nasal congestion: Nasal decongestantA void prolonged use to prevent rebound congestion. Drugs: Nasevion drop (Merk), Otrivin nasal drop (Novartis) b . Sore throat aspirin (con- traindicated in children below 16 year to prevent Reye s syndrome). Acetaminophen Xylocaine viscous 2% as g a r gle, warm saline gar gle. T antum oral rinse (elder) c . Cough: Codeine linctus indon. Dextromethorphan15- 30 mg 8 hourlyGlycodeine (Alembic), eltuss (Elder), grilinctus (Francho India) Ribavirin (see table 1 1.2) Amantadine Rimantadine Personal hygiene. Hand washing. A void contact Same as above Same as above Influenzal vaccine specially contd...

Treatment of Fungal Infection of Lungs 12 L ung and Pleura TREATMENT OF FUNGAL INFECTION OF LUNGS The treatment includes medical (antifungal drugs), sur gical and preventive therapy . Table 12.1: Diseases, antifungal therapy, surgical therapy and prevention P r evention Hydrated lime and sodi- um hydroxide kill fungi in droppings of pet pigeon. Diseases Candidiasis Cryptococcosis ( T olurosis) Antifungal therapy Localised Disseminated and disease invasive disease  Flucytosine 100 mg per kg per day orally in 4 divided dosages + Amphotericin-B pare- nteral Or Ketoconazole + Fluconazole (oral or IV) also ef fective Progressive form, meningitis: a. Amphotericin-B total dose 1-3 gm b . Amphotericin-B intrathecally in meningitis c. Amphotericin-B 0.4 mg/kg + 5-Flucytosine 150 mg/kg in divided dosages. Side effects: V enous thrombosis Local amphotericin-B or nystatin Fluconazole oral contd...

Respiratory Failure 13 L ung and Pleura ACUTE RESPIRATORY FAILURE Diagnosis History Dyspnoea, cough, sputum, fever . History of fume inhalation, trauma to chest and central nervous system. Physical Examination Altered sensorium, confusion open mouth panting, jaw tug, tightening and pursing of lips, hypercapnia, flaring of ala nasi, sweating, central cyanosis in mucosa of lips and tongue, muscle twitching, tremor . Investigations i. Arterial blood gas: PaO 2 less than 60 mmHg, PaCO 2 above 49 mmHg. ii. Arterial pH below 7.3 with hypercapnia. iii. Chest radiograph: Look for pneumonia, fluf fy shadows of adult respiratory distress syndrome, hyperinflation of chronic obstructive lung disease, cystic shadow of bronchiectasis pleural ef f u - sion, pneumothorax, infiltra- tion and chest cage defor- mity . iv . Bacteriological examination of secretion. v . Examination of blood and urine. vi. Investigations for evaluation of CNS and CVS. Management Goals of tr eatment: A . Maintenance of airway B . Administration of oxygen C . T reatment of infection D .

Treatment of Pleural Disease: Effusion and Empyema 14 L ung and Pleura Exudate Protein: 3 gm/dl or more LDH: Above 0.6 Sp. gravity: 1016 Cells: Acute infection  polymorph excess, chro- nic infection  lympho- cytes excess T ransudate Low protein, low LDH, low sp. gravity Causes: CCF , cirrhosis, myxo- edema, Meigs synd- rome, sarcoidosis Chylus Milky , no cell, chylomic- rons. Evidence of cancer lung and lymph gland with mediastinal spread DIAGNOSIS Clinical Manifestations Pain aggravated by respiration, fever , dyspnoea. Chest movement reduced, stony dullness, vocal fremitus and breath sound reduced. Investigations a . X-ray chest (P A view)dense opacity shadow in hemithorax; Lateral viewfor small and encysted ef fusion. b . Ultrasound for small ef fusion. c . CT scan for detecting hilar lymph nodes or tumour as the cause of effusion. d. Fibroptic bronchoscopy and pleuroscopy for establishing the aetiology in some cases. e . Pleural biopsy , scalene biopsy for the cause in some cases. DIAGNOSTIC FLOW CHART First dif ferentiate dif ferent types of pleural fluid. Bloody Evidence of pleural, lung and mediastinal malig- nancy contd...

Ischaemic Cerebrovascular Diseases 15 Central N e r v ous Sy st e m Ischaemic cerebrovascular diseases include cerebral infarction, cerebral haemorrhage cerebral embolism and TIA (transient ischaemic attack). CAUSES A . Cerebral infarction: 1. Cerebral thrombosis with or without atherosclerosis 2. Cerebral embolism due to: Congenital heart disease Acquired valvular disease Cardiomyopathy Myocardial infarct Endocarditis Mitral valve prolapse 3. Cerebral venous thrombosis and cortical thrombophlebitis. 4. Aortitis due to syphilis, tuberculosis, rheumatic, T akayasu disease. 5. Bleeding disorders. 6. Dissecting aneurysm of bracheo-cephalic vessels. B . Cerebral ischaemia: 1. TIA 2. Arterial hypotension 3 . Cardiac arrhythmia 4. Rare causes: Oral contraceptives, disseminated intravascular clotting, cerebral malaria. C . Cerebral haemorrhage: See chapter 16 Causes of str oke in young : V alvular lesion, mitral valve prolapse, arteritis, arterial anomalies. Diagnostic clues: Thr ee clinical syndr omes: A. Cer ebral thr ombosis Neurological deficit lasts more than 24 hours resulting from occlusion of major vessels, minor vessels as in hypertension or in lacunar infarct. See table 15.1 Stroke syndrome. B. Intermediate syndr ome: Neurological deficit clearing in 1-3 weeks. C. TIA ( T ransient ischaemic attack): Neurological deficit clears in less than 24 hours. See T able 15.1 Stroke syndrome.

Intracerebral Haemorrhage 16 Central N e r v ous Sy st e m COMMON CAUSES Hypertension Ruptured saccular aneurysm Ruptured arteriovenous malformation Bleeding disorders Ruptured mycotic aneurysm. DIAGNOSTIC CLUES Clinical Manifestations a . Headache, vomiting, nuchal rigidity without prodromal symptoms, followed by flaccid, are flexic sensory-motor paralysis with lethar gy or coma. b . Common clinical syndromes: Putaminal haemorrhage: Haemipaeresis, slurred speech, drowsiness, coma, ipsilateral dilated pupil and complete third nerve palsy . Thalamic haemorrhage: Hemiplegia, hemianaesthesia, eyes displaced downwards and medially Pontine haemorrhage: V ery rapid coma, pupils miotic but reacting to light, quadriplegia. Cerebellar haemorrhage: Recurrent vomiting, truncal ataxia without haemiparesis, occipital headache, vertigo, forced deviation of eyes to opposite side, bifacial weakness, stupor . Laboratory Investigations a . CT scan showing site and size of clot, hydrocephalus, oedema, tissue shift and ruptured blood into ventricle. b. MRI more reliable. c . Arteriography excludes aneurysm, arteritis and angioma. d. EEG and skull X-ray not very helpful. e . Platelet count and coagulation studies should be done. TREATMENT 1. General supportive measures: See treatment of ischaemic cerebrovascular accident. 2 .

Subarachnoid Haemorrhage 17 Central N e r v ous Sy st e m FACTS YOU CAN USE FOR THE TREATMENT PURPOSE Subarachnoid haemorrhage is usually due to bleeding from surface arteries of brain. Important aetiological facts: Ruptured aneurysm: Congenital berry aneurysm (most common) mycotic aneurysm. A V malformation. Intracerebral haemorrhage with extension to subarachnoid space. V asculitis. Infection (TB, syphilis and bacterial). Incidence: Eighty-five per cent of congenital cerebral aneurysm are found in the anterior half of the circle of W illis rupture usually occurs at branches or bifurcation: Anterior communicating anterior junction in 29% and posterior communicating internal carotid in 28% cases, middle cerebral bifurcation in 18%, intracranial carotid bifurcation in 8% and vertebro-basilar bifurcation in 3% cases. DIAGNOSTIC CLUES Sudden excruating headache with or without vomiting and a brief period of unconsciousness followed by lucid interval or a restless state with confusion, paucity of focal signs, normal blood pressure and presence of nuchal rigidity . Occasionally , focal signs occur depending on the vessel involved: Arteries involved Clinical featur e s a . Posterior communicating aneurysmal bleed Ipsilateral 3rd nerve palsy (most common) b. Anterior communicating aneurysm rupture T ransient weakness of legs with pyramidal signs and akinetic mutism c .

Epilepsy and Seizures 18 Central N e r v ous Sy st e m FACTS YOU CAN USE FOR TREATMENT OF EPILEPSY Precipitating Factors of Seizures I. Disease: Hyperpyrexia, infection (encephalitis, meningitis, cerebral malaria, toxoplasmosis, cysticercosis, AIDS), brain abscess, intracranial SOL, CV A, metabolic and electrolytic disturbances, hyponatraemia, hypoglycaemia, hyper glycaemia, hypocalcaemia (less than 7 mg/dl), hepatic failure, uremia, hypertensive encephalopathy , toxaemia of pregnancy . II. Drugs: Isoniazid, chloroquine, strychnine, lead, alcohol, withdrawal of antiepileptic drugs. III. Others: Emotional stress, physical and mental exhaustion sleep deprivation, visual stimulation (flickering of light, television viewing), hot water , loud noise, music.

Parkinsons Disease (Paralysis Agitans) 19 Central N e r v ous Sy st e m AETIOLOGICAL, PATHOLOGICAL, AND CLINICAL FACTS WHICH YOU CAN USE FOR MANAGEMENT Aetiology A . Idiopathic (Paralysis agitans) B . Secondary: Postencephalitic parkinsonism Atherosclerosis Drugs and poisons: Reserpine, metoclopramide, tetrabenzine, tetrahydropyridine, manganese, carbonmonoxide poisoning Association with certain diseases Creutzfeldt-Jakob disease, Huntington s chorea.

Treatment of Other Extrapyramidal Disorders 20 Central N e r v ous Sy st e m DYSTONIA Aetiology of Dystonia A . Idiopathic B. Secondary: W ilson s disease, spastic disease, basal ganglia calcinosis, Parkinson s disease, Huntington s chorea, kernicterus, cerebrovascular disease, encephalitis, toxic level of manganese, L-dopa. Idiopathic dystonia: Characteristics Characterised by sustained muscle contraction resulting in twisting and abnormal posture Juvenile dystonia: Focal and segmental idiopathic dystonia: Charac- terised by a . Cervical dystonia: T orticollis-rotation of head to one side b . Cranial nerve dystonia: Blepharospasm, involuntary mouth opening and jaw clinching, tongue protrusion, dysarthria, dysphasia, harsh hoarse voice T r eatment T reatment unsatisfactory a . High dose anticholiner gic therapy: T rihexy- phenidyl 20-50 mg/day b. Other drugs: Beclofen, tetrabenzine, benzo- diazepam (clonazepam) and dopamine antago- nist pimozide 6-25 mg/day c . Severe dystonia: i . T etrabenzine 75 mg/day + Pimozide 6- 25 mg/day + High-dose anticholiner gic ii. Stereotactic thalmotomy d .

Multiple Sclerosis 21 Central N e r v ous Sy st e m Aetiological facts and diagnostic clues you want to know for divising rational tr eatment: Aetiology: Unknown, suggested theories: A . Genetic susceptibility: As evidenced by significant association of MS with HLA-A3, HLA-B7 and HLA-DWZ. B . Environment: V iral agent implicated but not confirmed. Diagnostic clues : Clinical features: I . General: Y oung adult suf fer most20-40 year is the most important age. Rare under 10 years and above 50 years. Frequency , u r gency , or hesitancy of micturition are fairly common. Relapses and remission are frequent. I I . Focal signs: Site involved Manifestations 1. Optic nerve a . Optic neuritis with sudden loss of vision in one eye which improves b. Optic atrophy with temporal pallor 2. Plaque in midbrain and pons Internuclear ophthalmoplegia. Diplopia 3. Plaque in cerebellum Scanning speech, nystagmus, and intention tremor 4. Plaque in spinal cord: a . Pyramidal tract Monoplegia, paraplegia, hemiplegia b. Posterior column Impairment of position and joint sense. Electric current like sensation radiating through the body (L Hermitt s sign) due to lesion of posterior column in cervical cord. c . Spinothalamic tract lesion Pain and temperature sensation dissociation. Laboratory investigation : No investigation is diagnostic. a . CSF: Shows nonspecific changes. b. MRI: Plaques can be demonstrated but not diagnostic.

Alzheimers Disease 22 Central N e r v ous Sy st e m A progressive type of dementia. Aetiological and pathological factors, clinical featur es you will need for devising rational tr eatment: Aetiology : Unknown, suggested theories: A . Environmental factors: Nutritional factors, infection, toxin, etc. B . Genetic susceptibility: Evidence: All patients of Down s syndrome develop Alzheimer s changes in the brain. Pathophysiology : Progressive neuronal degeneration of selective cells in the association and memory areas of cerebral. Cortex especially the lar ge pyramidal cells of the hippocampus, the amygdala and the parietal and frontal association areas.  Leads to secondary degeneration of ascending cholinergic and adrener gic pathways Diagnostic Clues Clinical featur e s : 1. Age: Presenile, before age 65 year; senileafter age 65 years up to 90 years. 2. Impairment of higher mental function: Impairment of vocational activities, managing finances and finding direction in public places. Memory disorder especially of recent memory . Aphasia, agnosia and apraxia. 3 . Impairment of vegetative function: T asks of daily activities such as eating, sleeping, bathing, dressing and continence are impaired. Investigations : Done for dif ferentiating other causes of dementia. a . EEG: Provides indications towards metabolic and toxic aetiologies of dementia. b. MRI: Used to exclude vascular , demyelinating, infectious and space occupying aetiologies of dementia. Treatment Symptomatic Treatment Symptoms T r eatment Insomnia T iclophos 500 mg at bedtime Repetitive behaviour Benzodiazepine or phenothiazine Incontinence a . Periodic voiding b. Incontinence devices or intermittent catheterisation c .

Meningitis (Pyogenic) 23 Central Nervous System Facts you can use for tr eatment purpose: A . Or ganisms responsible for bacterial meningitis and age: Or ganisms Age gr oup Neisseria meningitidis Most common in first year of age Haemophilus influenzae Most common in children S t r eptococcus pneumoniae Most common in adults B . Predisposing factors: Upper r espiratory tract Lower r espiratory tract Others infection infection Sinusitis Pneumococcal pneumonia Alcohol Chr onic otitis media Closed head injury Mastoiditis Sickel cell disease Asplenism C . Pathogenesis: Infection of CSF due to lack of immunity  Infection and inflammation of subarachnoid space injuring cranial nerves, spinal roots and adjacent blood vessels by purulent exudates  Obstructing flow of CSF resulting in hydrocephalus DIAGNOSTIC CLUES Clinical Manifestations Common features : Fever , vomiting, impaired consciousness, headache, stif fneck and back with special characteristics due to dif ferent of fending or ganisms and age group as follows: Age gr oup Or ganisms a . Children: Fever and vomiting more a . Meningococcal meningitis: Petechial or purpuric frequent than headache. Seizure common. rash 50% patients Classical signs of meningism minimum b. Elderly: Signs of meningeal irritation b.

Brain Abscess 24 Central N e r v ous Sy st e m Aetiology A . Primary sources of infection: a . Ear: Otitis media b. Paranasal sinus: Sinusitis c . Metastatic and haematogenous spread: Bronchiectasis, lung abscess, empyema, congenital heart disease with right to left shunt such as T etralogy of Fallot associated with septicaemia, endocarditis d. Penetrating injuries of head and face. B . Or ganisms: Anaerobes, S taph. aur eus, S tr ep. pneumoniae, S tr ep. viridans, S tr ep. pyogenese, Haemo- philus influenzae, Enter obacteriaceae, E. histolytica . Diagnostic Clues Clinical manifestations: Evidence of primary source of infection, features of space occupying intracranial lesion (features of raised intracranial pressure such as headache, vomiting and impaired consciousness, focal neurological signs such as hemiplegia, seizures). Laboratory Investigations a . X-ray skull (gas), sinuses, mastoid and chest (lung abscess). b. CT scan or MRI: Lucent area with dense rim with shifting and compression of ventricle. c . EEG: Focal abnormalities. d. Leukocytosis. Treatment A . Symptomatic treatment: Urea, mannitol or dexamethasone for reducing raised intracranial pressure and cerebral oedema. Dilantin sodium for seizure. B . Medical therapy: a) If culture not available: Penicillin 4 mega units 4 hourly with gentamicin (80 mg 6 hourly) and chloramphenicol (4-6 gm/day) or metronidazole 500 mg 6 hourly cefotaxime 12 gm/day . S tart with IV followed by oral medication. C . Sur gery: a . When medical treatment fails and progression and persistence of intracranial pressure manifested by deepening coma needs operative intervention. b. Mastoidectomy and drainage of the frontal sinus should be done in case of otitis media and frontal sinusitis. c . In osteitis of skull bone: Af fected skull bone should be removed.

Myasthenia Gravis 25 Central N e r v ous Sy st e m Aetiological and Clinical Features you must know for Divising Rational Treatment Aetiology : Pathogenesis : Myasthenia gravis is an acquired autoimmune disorder  Formation of antibodies to acetylcholine receptors of neuromuscular junction  Cause complement mediated damage to the neuro- muscular junction  Neuromuscular transmission af fected  Leads to fluctuating weakness of voluntary muscle (essential feature of myasthenia) DIAGNOSTIC CLUES Fluctuating weakness of voluntary muscles: Muscle involved Manifestation i. Extraocular muscles  Ptosis, diplopia, strabismus ii. Facial muscles  Dif ficulty in eye closure, whistling, smiling, pouting lips and chewing iii. Bulbar muscles  Dysphagia iv . Laryngeal and  Low voice, nasal voice respiratory muscles v . Neck muscle  Usually extensors of neck are involved vi. Limb muscles  Proximal muscles of upper limb frequently involved Evidence of autoimmune disorder: i. Antibodies to acetylcholine receptors of neuromuscular junction found in 90% patients i i . Strong association between HLA B8, BW 35 and B21 antigens with Myasthe- nia gravis iii. Thymoma or thymic hyperplasia is associated with myasthenia.

Headache 26 Central N e r v ous Sy st e m Classification: A. Idiopathic or primary headache: a . Migraine: i. Common migraine (90% cases) ii. Classic migraine b. T ension headache : i . Episodic i i . Chronic c . Cluster headache B. Secondary headache: a . Intracranial causes: i. V ascular headache: Cerebrovascular accident, Subarachnoid haemorrhage, venous thrombosis. ii. Nonvascular headache: High CSF pressure, low CSF pressure b. Metabolic and hypoxic headache: i. Sudden ascent to altitude above 3000 ft ii. Chronic pulmonary disease iii. Sleep apnoea syndrome c . Reflex headache: i. Cervical spine disorder ii. Eyes: Acute glaucoma, refractive error iii. Nose and sinuses: Sinusitis iv . T emporomandibular joint disorder d. Neuralgias: i. T rigeminal neuralgia ii. Glossopharyngeal neuralgia iii. Occipital neuralgia iv . Atypical facial neuralgia C. Miscellaneous headaches: i. Cold stimulus headache ii. Benign cough headache iii. Benign exertional headache iv . Headache associated with sexual activity v . Hypertensive encephalopathy vi.

Treatment of Certain Neurological Symptoms and Diseases Not Already Described 27 Central N e r v ous Sy st e m Symptoms and diseases 1 . Raised intracranial pres- sure 2. T o reduce raised intra- ventricular pressure in mild hydrocephalus 3. Dementia T r eatment i. Mannitol (20%) 1 10 ml 4-8 hourly IV ii. Glycerol (10%) IV 1 to 2g/kg over 4 hours iii. Dexamethasone 12-20 mg/24 hours a. Acetazolamide reduces secretion of CSF by inhibiting enzyme carbonic anhydrase b. Oubain, isosorbide and frusemide also reduce CSF secretion c . Oral glycerol is also used successfully d . Progressive postmeningetic hydrocephalus of tuberculous origin can be helped by intrathecal corticosteroid or hyaluronidase apart from tuberculous chemotherapy e . Hydrocephalus of pyogenic meningitis origin helped by antibiotics i. For sleep: T riclofos 500 mg at bedtime ii. Incontinence: Periodic voiding, incontinence devices, intermittent catheterisation. iii. Repetitive behaviours: T ranquilisers, e.g. short acing benzo- diazepines or phenothiazines iv . E r got alkaloids may improve mood v . Choliner gics: Acetylcholine precursors, choline and lecithin coadministered with piracetam have some beneficial ef fects vi. Physostigmine sometimes used to improve overall function vii. Centrally active acetylcholinesterase inhibitors, such as tacrine in dosages up to 160 mg daily may benefit viii. Experimental drugs: Drugs which may directly stimulate postsynaptic acetylcholine M1 receptors and block presynaptic autoregulatory acetylcholine M2 receptors, and thus maximizing the ef fect and release of the cognitively important neurotransmitter .

Psychiatric Disorders 28 Central Nervous System SCHIZOPHRENIC DISORDERS Aetiological, pathophysiological and diagnostic clues: Aetiology and pathophysiology : Unknown. An abnormality in functional integration of sensory and cognitive information exists in schizophrenia. Suggested theories: A . Genetic factor: 10-15% of of fspring of a schizophrenic parents at risk for the disease B . Biochemical factor: Altered dopamine metabolism resulting in excess dopamine in basal ganglia may be responsible. Diagnostic Clues Clinical features: Delusion ++++; hallucination ++++; incoherent speech ++++; depressed mood; grandiosity ++. Prodromal symptoms: Marked social isolation; markedly peculiar behaviour (collecting garbages, talking to self in the public); hoarding of food. Recurrent illusions: Sensing the presence of a force or a person not actually present. TREATMENT Drug Therapy Neuroleptics Remarks i . Drugs such as benztropine mesylate (cogentin), diphenhydra- mine HCl (benadryl) and trihexy- phenidryl artane are added to neuroleptics to prevent extra- pyramidal side-effects. ii. T ardive dyskinesia: No effective treatment is available. Gradually decrease the dose of neuroleptics Do Do Do Drugs Daily dose Range (mg) I. Phenothiazines a. Chlorpromazine 300-800 b . Thioridazine 150-800 (melleril) c. Perphenazine 8-60 mg d . T rifluoperazine 4-60 Side-effects i. Extrapyramidal side-ef fects i i . T ardive dyskinesia: Choreo- athetoid movements involving mouth, lips, tongue, limb, and trunk. Frequent early sign is vermicular movement of tongue Do Do Do contd...

Affective Disorders (Depression) 29 Central N e r v ous Sy st e m CLASSIFICATION TREATMENT T reatment of major depression: Drug therapy: Antidepressant drugs: Drugs Daily dose Side-effect s RemarksAdvantages range (mg) Appetite Sleep Energ y Self-esteem W eight Concentration Hope Agitation or Retardation Mania Psychotic Symptoms like schizophrenia Or ganic aetiology of symptoms Major depr ession Poor or excess Insomnia or hypersomnia Loss of ener gy or fatigue Feeling of guilt Significant weight loss or gain Poor a . Loss of interest in all activi- ties b . Suicidal tendency Present No manic swing At least present for 2 week period Duration No Minor Depr ession Same as major depression Do Do Low Not much Poor Pessimism Usually not marked Never had manic episode At least for two years duration during which there has been depressed mood most of the day No A . T ricyclic or tetracyclic antidepr essants: Imipramine 150-300 Anticholiner gic side-ef fects, sedation, hypotension, cardiac (palpitation, tachycardia, depres- sed ST segment, flattened T , Imipramine and desipramine are alerting antidepressant, useful in patients with retardation and hypersomnia less anticholiner gic side-ef fects.

Grief Reaction 30 Central N e r v ous Sy st e m Relatives of patients who died show depressed mood, sleep disturbances and crying lasting for two to six months. Panic attack may develop. Supportive tr eatment by physician himself: i. Share his feelings. i i . Review the relationship of the decreased with the important people in their lives. iii. Find new persons with whom the bereaved can develop relationship. iv . Suggest to the bereaved measure to combat stress v . Or ganise support groups. Medications: i. T reat depression with antidepressant drugs. ii. T reat panic disorder . See further . iii. Mild sedation and hypnotics may be needed. Suicidal Tendencies Suicide is high in: i. Depressed patients i i . Alcoholics iii. Schizophrenics Diagnostic clues: i. Age 20-45 years more prone to suicidal tendencies. ii. W idows, divorced, solitude, unemployed or retired iii. Enquire whether they have had thoughts about death or suicide (better of f dead or people would be better of f without me). iv . Preoccupation with funeral, cemetery , burning ghat v . Planning to buy weapons vi. Patient agitated or depressed Management: i. Need psychiatric consultation ii. Arrange for supportive environment iii. A void prescribing heavy dosages of sedatives, hypnotics and antidepressants. Inspite of physician s instruction the patient may take them in excess dosages.