CIRCLE OF WILIS

TRIGEMINAL NEURALGIA

.Occurs in elderly ,etiology is unkwn,may b due to vascular compression at root entry zone of 5th nerve.
.C/F=
.Paroxymal,sharp pain ,confined to distibution of nerve.Maxillary nd mandibular division commonly affected
.Pain is ppted by touching triggeq zones eg cold wind blowing on face,washing fabe ,chewing or talking
.No abnormalities of 5th nerve functn seen on physical examinatn
.Pain of trigeminal neuraglia differ frm pain following reactivatn of varicella zoster virus
.Similar type of pain occur in
multiple sclerosis ,basilar aneurysm ,cerebral tumour

.TREATMENT=
.Carbamazepine start with 100-200 mg/day,increase in 2-3 wks to 200-400 mg tid
.Phenytoin 100 mg tid
.Clonazepam 1-2 mg tid
.Localised pain managed with injectn of phenol or alcohol

STATUS EPILEPTICUS

1. Clinical diagnosis-
a) 2 fits occur without recovery of consciousness in between.
b) a single fit lasts longer than 30 minutes even without loss of consciousmess.
2. Fatal condition

CLASSIFICATION-
2 types mainly.
a. Generalised
b. Partial


a. Generalised further divided into convulsive & non convulsive.
b. Partial includes partial motor seizures.

CAUSES -
1. Sudden antiepileptic withdrawl
2. Metabolic disorders - hypoglycaemia,hypnatremia
3. Infections- encephalitis, meningitis
4. Brain tumor or trauma



TREATMENT
Control seizures first them underlying cause.


 step A
 ¤  first 20 min
 ¤ maintain airway
 ¤secure proper IV & draw blood for metabolic para
¤ briefe history
¤conduct rapid examination to determine focal signs, increased intrac tension.
¤administer diazepam 10 - 20 mi IV over 1-2 min & SOS every 10 min followed by loading dose of diphenyl hydantoin 18-20 mg per kg at a rate of 50 mg per min. Total ford should not exceed 1.000 mg this should control seizure in 20 min. If not then

STEP B-
¤20-60 MIN
¤phenobarbitol 20 mg per ki IV or diazepam infusion 2-4 mg per hr may require assisted ventilation. If not controled with this


STEP C

¤general anaesthesia for pentothal infusion
¤ simultaneously b.p,acidosis, ventilation & electrolyte balance
¤ago to control seizure within 1 hr after admission.


MANAGEMENT OF CONVULSIVE STATUS EPILEPTICUS

1) 0-5 min

 ¤maintain airway, breathing,& circulation
¤administer oxygen
¤insert iv line
¤obtain blood samples for glucose ,urea , electrolyte, bilirubin , toxicology
¤ administer glucose if hypoglycaemia

2) 5-20 min

¤administer diazepam
¤administer phenytoin
¤repeat diazepam
¤evaluate for intubation


3)20-60 min

¤administer phenobarbital
¤support of respiration
¤conduct detail examination

4) >60 min
¤ consider paraldehyde or lidocaine
¤intubate & ventilate
¤ administer general anaesthesia
¤ admit in ICU.

Narcolepsy:

Narcolepsy:
  It is a disorder charactorised by excessive day time sleepiness, often disturbed night time sleep and disturbances in the REM sleep.
  Decrease REM latency is the hallmark; REM sleep occures within 10 mins of onset of sleep.
  Common age of onset is 15-25 yrs and continues thoughout the life.

Tetrad of symptoms:
 1) sleep attacks:
    - Person is unable to resist a sleep (nap)
    - attack occures during nytime of the day
    - gap of 2-35hrs betn two naps
 2) cataplexy:
    - char' by loss of muscle tone in various parts of body. e.g. Drop jaw
    - may b precipited by sudden emotion
 3) hypnagogic hallucinations:
    - dreal like vivid perceptions which occures at the onset of sleep and associated with fearfullness
    - these occuring at the time of awakening r called as hypnopompic hallucinations
 4) sleep paralysis:
    - this occures either at awakening or at sleep onset
    - person is concius bt unable to move his body
    - episode last for 30 sec to few mins



Other associated symptoms r:
 Fugue states, blackouts, blurring of vision,

Diagnosis: confirmed by polysomnography which shows decreased REM latency

Treatment:
   - forced naps at regular times in the day
   - stimulant medicatin e.g. Amphetamine or modafinil
   - anti-depressants

LUMBAR PUNCTURE

   * Indications
 A) Dignostic
 - absolute
 1) meningitis
 2) encephalitis
 3) subarachnoid hadmorrhage
 4) GBS
 5) acute  demyelinating disease
 6) transverse myelitis
 7) unexplained coma
 8) unexplained dementia

 -Relative
 1) multiple sclerosis
 2) PUO
 3) neurosyphilis

    B) Therapeutic
 1. Methotrexate in leukaemia
 2. Spinal anaesthesia
 3. Benign intracranial HTN

 
   *CONTRAINDICATION
 1. Raised intracranial
 2. Spinal deformity
 3. Local infection
 4. Coagulation disorders

GULLAIN- BARRE SYNDROME(GBS)

GULLAIN- BARRE SYNDROME(GBS)=  . GBS is commnest acute polynetropathy.  It affects people at any age.   Usually follows viral infection.  PATHOLOGY= 1-it is a monophasic immunologically mediated inflammatory disorder of peripheral nerve. 2-multifocal demyelination with inflammation results in coduction block. 3-severe forms show sec. axonal degeneration. CLINICAL FEATUSES= 1- acute disorder, progress for few days. 2-predominent motor neuropathy. 3-distal paraesthesias wid mildly disturbed joint postion sense. 4- motor paralysis is more striking n symmetrical, involving proximal muscles. It begins in legs, progressing over several days to involve arms, face n eyes.   5- reflexes r absent. 6- bulbar muscle weakness. 7- resp. paralysis n autonomic disturbances  occur in few.
INVESTIGATIONS= 1-CSF show raised proteins,..2-nerve conduction velocity is slow.    3-acute intermittent porphyria, post-diptheritic neuritis n drug induced acute polyneuropaties have to b ruled out.   TREATMENT= 1-maintainance of airway, breathing n circulation.  2-ventilate if pt. feels resp. failure.  3- monitor pulse, blood pressure, cardiac activity using a cardiac monitor if pt have instability. 4-plasmapheresis n gamma-gloubulins 0.4 g/kg/day for 5 days. 

BELLS PALSY

Aetiology
herpes simplex virus and herpes zoster
PATHOLOGICALLY
odema and swelling of the nerve accur witho facial canal ,often at stylmastoid foramen
CLINICAL FEATURES
FEATURES OF LMN PALSY
1 PARALSIS OF ALL THE MUSCLES OF ONE SIDE OF THE FACE
2.Drooping of the palsy ,effacement of creases and skin dole on affected side .
3.weakness of frowning and eyes closures the upper facial muscles are weak .
4. Drooling of saliva from angle of mouth .
5. On asking the patient to show his teeth ,the angle of the mouth deviates away from the side of lesion
6.upon attempted closure of the eyelid .
the eye on the paralysed side rolls upwards .
7. Corneal ulceration due to inability to close the eye during sleep.

,
INVESTIGATION
1. ELECTROPHYSIOLOGICAL test
2. To rule out alternate diagnosis , appropriate diagnostic procedures may be necessary.
,,
TREATMENT
PREDNISOLONE AND ACYCLOVIR
-Prednisolon 1mg/kg /day for 1st wits the dosage tapering off over the 2nd week.
- Aciclovir at a dosage of 800mg five times a day for 5days.   ,
 

TREATMENT OF STATUS ASTHAMTICUS

TREATMENT AT HOME.
1.high concentration. Of oxygen through M.C mask.  2.Bronchodilator theraphy with one of the following :
-Salbutamol 5mg or terbutalin 10mg by nebuliser every 20 min for 3 doses.
-Salbutamol or terbutalin administered by metered dose inhalers.
-aminophylline 5mg/kg I.V over 20 min.
3.Corticosteroid theraphy.
-hydrocortisone sodium succincte 200mg I.V
-methyl prednisolone 125 mg i.v.

TREATMENT IN HOSPITAL.

1.High concentration oxygen.
2.Salbutamol 5mg or terbutalin 10mg by nebuliser every 20 min for 3 doses.
3.Subcutaneous or I.V administration of beta-2 agonist in patients who have excessive cough.
Adrenalin 0.2-0.5 mg as 1:1000 solution subcutaneous every 20 min.
4.Ipratropium bromide 0.5 mg together with salbutamol 5mg ,if patient does not respond in 15-20 min.
5.Aminophylline I.V if no responce to nebulised bronchodilator.
6.Corticosteroids
-hydrocortisone sodium succinate 200-500 mg intravenously.4 to 6 hourly.
-oral prednisolone, loading dose 40-60 mg and there after 20 mg 6 hourly.
7.Endo tracheal intubation And mechanical ventilation in case of respiratory failure, severe hypoxia,acidosis.
8.Non invasive ventillation using continuous positive pressure or bi -level positive airway pressure. It reduces the work of breathing.
9.70% helium with oxygen reduces airway resistance and improves efficacy of broncho dilators.
10.Response is assessed from patients distress, respiratory rate ,heart rate and serial artericl blood gas studies.

SCHIZOPHRENIA

Symptom of act variety positive symp

delusion
hallucination
interference with thinking

Symptom of chr variety negative symp

apathy
lack of drive
slowness
social withdrawal

act syndrom
1 behaviour variab
2 spech vage misterical idea
3 disorder of stream of thought
4 loss of association
5 mood abnormal
6 visual auditar hallucination
7 delusion



chr syndrom
1 diminished volition
2 motor disturbance
stupor
excitement
waxy flexibility
catalepsy

Schneider's symp of first rank
1 hearing thought spoken aloud
2 third person hallucinatio
3 hallucination in form of commentary
4 somatic hallu
5 thought withdrawal or insertion
6 thought broad casting
7 delusional perception

Aetiology

1 genetic
2 family problem
3 physical illness
4 psycosocial stress
5 social isolation
6 occupation
7 disturbance of neurotransmitor fun:- dopamine hypothesis
8 transmethylation theory
9 5ht def

Type
1 simple
2 hebephrnic
3 catatonic
4 paranoid

Management
1 drug
chlorpromazin dose 300 to 1000 mg /d
trifuloroparazin 15 to 25 mg./d

sideeeffct
extrasyramidal reaction

2 Ect
3 Behaviour therapy
4 occupational therapy

MYASTHENIA GRAVIS

@Autoimmune disorder in which antibodies (Ab) against acetylcholine [Ach] receptors at motor end plates in NM junction.
@ Ab production by B cells defectively regulated by T lymphocytes
@ increased incidence in thymoma pts

C/F
@ Age- 15 to 50 yr
@ females more affected
@ easy fatiguability with muscle paresis
@ reflexes, sensations normal
@ diurnal variations present
@ ocular muscles most commonly affected resulting in Ptosis n diplopia. Pupils not involved
@  bulbar muscle Involvement results in dysphagia, nasal regurgitation n nasal twang
@ proximal Limb muscles involved - difficulty in raising hand above head n problems in getting up 4m squatting or sitting positions
@ involvement of respiratory muscles results in myasthenic crisis can cause death



Myasthenic crisis
@ in pts with MG not on any Rx or drug resistant

Cholinergic Crisis
@ Result of relative overdose of anticholinesterases drugs presents with diarrhea excessive salivation n lacrimation, resp insufficiency urinary incontinence

Investigations

# Tensilon (edrophonium) test
@ it is anticholinesterase inhibitor short duration action
@ 2 mg as test dose followed by 8mg results in dramatic improvement in symptoms within 30 sec n persists up to 1 to 2 minute suggestive of MG

# Others
@ CXR n CT 4 thymic enlargement
@ thyroid function test [10% postive]
@ Ach receptor Ab levels [in > 90% pts]
@ Anti muscle specific protein kinase Ab
@ nerve conduction test, repititive nerve stimulation,  exercise testing, single fiber EMG
@ Ice test
patients with ptosis small cube of had placed over eyelid 4 2 min - improvement suggest disease

Management

# Anticholinesterase
@ neostigmine (15mg) or pyridostigmine (75mg) 3 to 6 times a day
side effects like abdominal cramps managed with propantheline 15 mg BD or tds

# Steroids
# Thymectomy
# Immunosuppression by azathioprine cyclophosphamide mycophenolate
# Plasmapheresis n IV Ig 4 short term remission
# Supportive measures
ventilatory assistance n nasogastric tube

INVOLUNTARY MOVEMENTS

Involuntary movements usually imply a disorser in basal ganglia.

Movement dissorders:
1) parkinsonism  - lesion at sustancia nigra
2) chorea - caudate nucleus
3) hemibalismus - subthalamic nucleus
4) myoclonus - different areas

Drugs causing tremors:
- nifidipine
- nicotine
- lithium
- valproic acid
- tricyclic antidepressants
- antihistaminics
- thyroxine



Types of tremours.
1) rest or static tremors
      Typically sren in parkinsonism
2) postural tremors:
      Common in drugs like non selective beta
      blockers, also intramuscular inj of botuline
      toxine type A.
3) intension tremors:
      Typical sign of cerebellar lesion

CHOREA:
  Non-repetative jerky semipurposfull movements of
  face, trunk and limbs
  Causes:
     Rheumatic (sydenhams chorea)
     Huntington's chorea
     Hyperthyroidism
     SLE
     Hyperparathyroidism
  
   Rx:
     Symptonatic:
         - haloperidol 0.5-1.5 mg BD
         - sodium valproate 200-600 mg TID
         - carbamazepin
         - phenobarbitone
     In rheumatic chorea, penicillin prophylaxis

Myoclonus:
   It is rapid brief irregular movements of part of body.
 
Causes:
    - metabolic disturbance--eletrolyte imbalance
    - encephalitis
    - tricyclic antidepressant
    - lipid storage diseases
    - myoclonic epilepsy
  
  Rx:
    - sod valproate 300-1200 mg/day
    - clinazipam 0.5-10 mg/day
  

GAIT DISORDER

1.CIRCUMDUCTION GAIT.
-Seen in hemiparesis.
-Patient throws his leg outward, movement occuring at the hip joint, also leans towards opposite side.
-Affected arm is Adducted at shoulder and flexed at elbow, wrist and fingers.
2.SPASTIC GAIT.(bypyramidal gait)
-Seen in upper motor neuron involving both lower limbs.
-There is adductor spasm causing legs to cross each other and each foot trips the other ->scissor gait.

3.HIGH STEPPING GAIT.
-Seen in foot drop.
-Patient raises the foot high up to overcome the foot drop and on keeping the foot down the toe hits the ground first.



4. HIGH STEPPING AND STAMPING GAIT.
-Seen in posterior column lesion where ties is gross loss of position sense.
-patient does not know where his foot is and so while walking raises the foot high up and brings down on the ground forcefully like stamping..And the heel of the foot coming in contact with the ground first.

5.ATAXIC GAIT,
-SEEN in cerebellar lesion.
-Patient is ataxic and sway in any direction and walls with a broad base.

6.WADDLING GAIT.
-Seen in proximal muscle weakness of lower limbs or with bilateral hip problem,
-patient walk with broad base with exaggerated lumbar lordosis.

APHASIA

APHASIA= 1=SENSORY APHASIA- a) it is a disorder of language wid enability to encode or decode d signals used in d language.  b) sensory aphasia denotes dysfunction in afferent area, i.e. failure to comprehend verbal written messages.  c) lesions hn dominent post. perisylvian areas r responsible.  d) signs- poor comprehension of spoken speech n inability to read through person is able to hear n see.   e)types- 1-wernicke's aphasia( repetition is defective). 2- transcortical sensory aphasia( repetition is preserved).
 2=MOTOR APHASIA- a) it is disorder in efferent area.  b) lesions responsible r located in anterior perisylvian area.  c) comprehension is relatively well preserved.  d) spoken speech is non-fluent.  e) word out put is reduced., effortful, dysarthric n monosyllabic.  f)pt is able to communicate to some extent. g) types- 1-broca's aphasia.   2- transcorticak motor aphasia. 

Syringomyelia

Syringomyelia is a disorder where cavitation occur within spinal cord along with dilated central canal.
     Common sites - lower cervical & high thoracic region
      Many associated with Chiari malformations
  * Causes
1. Congenital (idiopathic)
2. Associated with  tumours
3. Post-traumatic
4. Arachnoiditis
   * C/f
1. Common in females
2. Occurs during 3rd  or 4th decade of life
3. Numbness in upper limbs with frequent burns & injuries which r painless
4. Spatic weakness in lower limbs with bladder involvement
  
*Signs
1. Scoliosis with central cord syndrome with following findings
  - LMN signs in upper limbs
  - Dissociated suspended ancestiesia
   - pyramidal signs in lower limbs    
2. Thoracic kyphoscoliosis is common
3.  Sensory disturbances may extend to neck & face
       *INVESTIGATIONS
1. Plain radiograph of cervical spine
2. Myoelogram
3. CT scan
4. MRI of brain & spinal cord shows fluid filled cavitation & dilated central canal . Most sensitive
       *TREATMENT
   Surgical removal of obstruction to CSF flow , along with syringo - subarachnoid shunt  

  
 

Parkinsonism

Parkinsonism is a syndrome consisting of akinasia and bradykinesia, rgidity and tremors.
  Usualyy associated with abnormalities in postural rightning reflexes

Pathology:
 - loss of pigmented cells in substantia nigra with      deposition le lewy bodyies
 - degeneration of nigro-striatal pathway
 - dopamine level in striatum gets depleted which is normally synthesised by pigmented cells

Clinical features:
 - both sexes equally affected
 - sixth decade
1) Tremors:
  
  - Tremors at rest which decreses with action
     - occures at wrist and fingers
     - may occure at head, jaw or lower limbs
     - tremors r charactoristically pill rolling
2) rigidity:
     - lead pipe hypertonia. Hypertonia is due to
       rigidity
3) hypkinesia/akinesia:
     - difficulty in initiating a motor act
4) bradykinesia:
     - pausity of movements
     - reduced movements
     - expressionless 'mask like face'
5) disturbed postural reflexes:
     - bent posture with tendancy to fall easily
     - difficulty in maintaining balance
     - glabellar tap becomes positive
     - may develop depression, dementia
     - autonomic symptoms like sweating, sebaceous
       secretions, urinary urgency and constipation
     - low volm, monotonus speech, stance is
       stooped, shuffling gait with absent arm
       swinging, turning about bcomes slow
     - with advancement pt assumes flexed posture,
       unable to move, death occures due to
        infections

Managment:
    If any offending drug was used, it shud b withdrawn

Drug therapy:
 (1) anticholinergic:
        Trihexyphenidyl, benzhexole r useful in controling tremors only. Cause urinary retension, worson glaucoma. Avoided if pts is above 65
 2) amantidine:
        Potentiates endogenous dopamine, hs mild antiparkinsonian effect.
 3) levodopa:
       - oraly afministerd Levodopa afr administration crosses bloodbrain barrier and gets metabolised to dopamine in the brain. Bt large amt gets metabolised peripheraly to dopamine. By combining peripheral decarboxylase inhibitor e.g. Carbidopa, bensarazide with Ldopa this can overcome.
      - Ldopa : carbidopa is 4:1
      - Ldopa : bensarazide 4:1
      - drug is started at low dose and increase  once in 2 wks
      - at higher doses A/E like dyskinasia and hallusination occures
 4) dopamine receptor agonist:
      - these r bromocriptine, lisuroid, pergolide used in addition or as alternative to Ldopa
      - bromocriptine 2.5 mg/day incresed slowly to 60 mg/day
 5) seligiline:
       MAO B inhibitor. Reduces metabolism of dopamine and reduces dose and frequency of Ldopa
 6) COMT inhibitors
      : tolcapone, and entacapone. Enhances Ldopa by reducing conversion of Ldopa to methyldopa

Surgery:
    Steriotactic thalamotomy and deep brain stimulation (subthalamic nucleus and globus pallidus) in sever diseases.

MULTIPLE SCLEROSIS

1-it is an autoimmune disease of white matter which occurs due to interaction of genetic factors with enviornomental factors
2:-most frequently affects young &middle aged people
3-characterised by chronic inflammation, demyelination axonal loss with remission &exacerebation of signs symptoms
Classification
1- Relapsing remitting multiple sclerosis 85%
it is characterised by signs &symptoms typicaly evolve over period of several days stabilise then improve spontaneously or in response to costicosteroids
2- secondary progressive multiple sclerossis
it is characterised by gradual progression of disability with or without superimposed replase
3- Primary progressive multiple sclerossis 10%
it is characterised by gradual progression of disability without superimposed relapse
4-Progressing relapsing multiple sclerossis 5%
it is characterised by gradual progression of disability from disease onset with or without relapse in the course of disease

C /F
1) Motor features
*predominately upper motor neuron weakness of muscles (brisk deep tendon reflex Babinski's sign, loss of abdominal reflex )
*wasting of muscles of hands
2)Sensory features
*tingling numbness
*objective sensory loss including posterior column features
3)Other features
*optic neuritis
*3rd cranial nerve palsy & worsening of symptoms on exposure to heat i.e Uthoff's phenomenon
4)Paroxymal features
*trigeminal neuralgia, facial weakness vertigo dysarthria
*Lhermitte sign- shooting electric pain in neck with radiation to shoulder on flexing neck due to posterior column involvement
Diagnosis
1- age of onset between 10 to 25yr
2- an acute episode must last for atleast 24 hrs in absence of fever
3- precence of prominent cortical sign exclude MS
MANAGEMENT
A) Investigations
1- csf- increased cells raised protein increased IgG
2- visual , auditary show prolongation
3-MRI is very sensitive
B) Treatment
1- Acute exacerebation - methyl prednisolone 1g iv daily for 3days.it is followed by oral prednisolone 60mg for 5days
2- disease modifying drugs- interferon beta.-1b,1a,mitoxantrone.
3- symptomatic treatment
spacticity - bacloèn(15to18mg /day , diazepam5-10mg/day
pain- phenytoin 300to 400mg/day
paroxymal symptoms- carbamazepine gabapentin or acetazolamide

Hydrocephalus

Hydrocephalus results from an imbalance between production and absorption of  cerebrospinal fluid.it may b communicating or non com.
A)in comm. There is on blockage between the ventricular system,the basal cisterns and spinal subarachnoid space.
B)in non comm. The block is at any level in the ventri. Systew commonly at d level of foramina of Luschka n Magendie.

Causes
1. Congenital
-intrauterine inf: rubella,cytomegalovirus,toxo.
-intracranial bleeds,intraventri hemorrhage
-cöng. midline tumours
-cong. Malformations:aqueduct stenosis,Dandy Walker synd.
2.acquired
-TB,chronic n pyogenic meningitis
-post intraventricular hemo.
-astrocytoma,ependymoma
-av malformation,intracranial hemo.,ruptured aneurysm



C/f
-enlarging head size
-delayed closure of sutures n fontanels
-headache,nausea,vomiting
-personality n behaviour disturbances.
-irritability,drowsiness,apathy
-papilledema,nerve palsies
-scalp veins dilated
-skull cöntour becomes abnormal.

Diagnosis
-cranial ultrasound
-CT Scan
-MRI

Management
-treatment of underlying disease -acetazolamide 50mg/kg/day
-oral glycerol
-ventriculo peritoneal shunt

DELUSION

DEF.
It is an irrationally held belief which cannot be altered in spite of evidence to d contrary.

PERSISTANT DELUSIONAL DISORDERS.
This category in ICD-10.

1. Delusional disorder(paranoid disorder)
it is characterized by following features.
i) persistant delusions must be present for atleast 3 months
#delusion of persecution i.e. Being persecuted against
#delusion of grandeur i.e. Inflated self esteem & self image
#delusion of jealousy i.e. Infidelity
#somatic (hypochondriacal) delusions
#erotomanic delusions (delusions of love)
#other non-bizarre delusions



2. Absence of significant or persistent hallucinations

3. Absence of organic mental disorders, schizophrenia & mood disorders.

-common cause appears to be an abrupt change in d environmnent & in immigrants.
-it is a disorder with usually stable & chronic course..
-it is characterized by presence of well systematized delusions of non bizzare type.
- the behavior outside d limits of delusion is almost normal.
- these individuals are able to carry on a near social & occupational life without arousing suspicion regarding d delusional disorder.
- when d content of delusion is predominantly persecutory it is important to differentiate it from paranoid schizophrenia & paranoid personality disorder.
- when d content of delusion is predominantly jealousy involving d spouse it is called as othello syndrome or conjugal paranoia
- when d content of delusion is erotic it is called clerambault syndrome.

OTHER PERSISTANT DELUSIONAL DISORDER.
These do not fulfill d criteria for delusional disorder.
1. Delusions associated with resistant hallucinatory voices.
2. Delusional disorder with a duration of less than 3 months.

TREATMENT.
1. Anti psychotics are used to control agitation & treat psychotic features.
2. Supportive psychotherapy.
3. Antidepressants &/or ECT maybe needed for secondary depression.

INDUCED DELUSIONAL DISORDER.
It is characterized by sharing of delusion between usually 2 or more persons who usually have a closely knit emotional bond. Only one person has the genuine delusions due to an underlying psychiatric disorder.

Anxiety

Anxiety disorder : classification 1anxiety state 2 phobic @ anxiety -panic disorder generalised anxiety post traumatic stress disorder @phobic-agoraphobia social phobia simple phobia 1 panic disorder- recurrent attack of severe anxiety r sudden and unpredictable physical attack prominent such as palpitation chest pain sweating chill nausea fear of dying numbness and feeling of detachment last for 1o 15 min 2 generalised anxiety disorder st have persistent excessive
unrealistic worry with other feature such as impaired concentration autonomic arousal restlessness and insomnia 3phobic persistent recurring irrational severe anxiety of sp object activities or situation with secondary avoidance behaviour of phobic stimulus  @treatment 1use of selective serotonin reuptake inhibitor 2selective serotonin nor epinephrine reuptake inhibitor eg venlafaxine 3anxiolytic agent benzodiazepine 4 cognative behaviour therapy          

SYNCOPE

Def....It consist of generalised weakness of muscle, los of postural tone, inability to stand upright and los of Consciousness
_fainting is lack of strength vth sensatiöns of impending los of los of consciousnes
_Faintness is podromal phase of fainting its characterisd by sequenc of event include Light headednes, blurring of vision proceeding to blackout, heavynes in lowr limbs and los of consciousnes

¤ MechanisM
_it s due to cerebral ischemia mainly to brain stem
_ischemia is due to sudden vasodialatiön and sudden fall in card. output

¤Types of syncope

1. Vasovagal syncope

_it is due to reflex slowing of heart mediated through vagus, and marked fall in arterial blod pres. And fall in PV resistance
_causes includ emotional stress, warm and ouercrowded room, sudden pain, mild blod los, anaemia, fever, fasting
.
.C/F
include prodromal phase characterisd by nausea, sweating, yawning, epigastric distress, tachypnea, weaknes, confusin. Ths s folowed by faintnes palor, coldnes of hand feet, weak pulse
_it s common in young people

2. Cardiac syncope

_it is due to sudden reduction in cardic output due to heart is beating to fast or to slow or nt at all
Causes
complte heart block, PSVT, sick sinus syndrome, MI, AS, PH, HCM, pul. Embolism, TOF

3. Orthostatic sncope
ths occur whn d person sudenly gets up 4m lying down position or stands still 4 long time
_basic mechanism is postural hypotensin due tn los of vasoconstrictor reflexes in lowr limb vessels
CauseS
PHysiological, idiopatihic orthostatic hypotnsn, anti hypertensive drugs, haemorrhage, diabetic neuropathy

4. Drug inducd SyncoP

_vasodialators/volume dplition e.g.ACE inhibitos, beta blocker, cc blockr, diuretics, nitrates
_arrhythmogenic
quinidine, amiodarone, TCAntidpresant

5.Miscellaneous cause of syncop
_vagal and glos6pharyngeal neuralgia
_micturition syncope in elderly pt
_cough syncope
_hypoglycaemia
_hyperventilation
_carotid sinus syncope