General neurology mine

Pathological reflexes occur during disease or failure of maturation of higher motor

centers. Thee reflexes usually only occur in developing nervous system. Maturation
of nervous system and higher cortical centers leads to suppression of these
reflexes.
Pathological Extensor reflex of foot
Pathological
Irritate
Reflex
Babinski
Irritate plantar external
edge
Oppenheimer
Stroke downward on
patients shin
Gordon
Squeeze calf muscle
Schaeffer
Press Achilles tendon

response

Extension of big toe with separation

of other toes

Plantar reflex is the norm in adults. Skin irritation of soles external edge = Toes flex
Pathological Flexor reflex of foot
Pathological
Irritate
Reflex
Zhukovski
Strike hammer on sole under toes
Rossolimo
Irritate sole at terminal phalanges of II-IV toes
Bechterew
Hammer on dorsal foot above III-IV metatarsal
bones
Pyramidal Pathway
Corticomuscular tract
Cell body in V layer of upper and
middle precentral gyrus:
90% of axons cross to other
side= pyramidal decussation
below the medulla;
these axons descend thru
lateral corticospinal tract
Lower motor neuron in anterior
horn of spinal cord:
Axons exit via ventral root
spinal nerves skeletal
muscles

response
Plantar
flexion

Structu
re
In.

Corticonuclear tract

IIn.

Motor nuclei of cranial nerves =

innervations of head and neck
muscles

Cell body in V layer of lower gyrus:

Axons approach motor nuclei of
cranial nerves from both sides
**only CN 12 nucleus and inferior CN
7 nucleus are innervated by opposite
hemisphere ONLY

Level of
damage
Symptoms

Central paresis
1st neuron or Upper motor neuron
(UMN)
Spasticity (increased tone with
initial resistance to passive
movement)
Hyperreflexia
Loss of superficial reflexes
Appearance of pathological reflexes
ie Babinskis
Defense reflexes
Knee and foot clonuses
Pathological synkinesia

Peripheral paresis
2nd neuron or Lower motor
neuron (LMN)
Hyptonia
Hyporeflexia
Muscular atrophy
Fasciculation (involuntary
muscle contraction and
relaxation)

Lesion of Pyramidal system

Level of Damage
Symptoms
Precentral gyrus
Damage = CL central monoparesis
Irritation = CL Motor Jacksonian epilepsy
Internal capsule
CL central hemiparesis
CL central paresis of CN 7 and 12
Wernicke-Mann posture= flexed upper limbs, extended
lower limbs
Brainst Cerebral
Alternating syndrome (AS):
em
peduncle
Webers syndrome = damaged CN 3 nucleus and
corticospinal tract;
SS diplopia, ptosis of upper eyelid, exophthalmus,
mydriasis, disturbed accommodation and convergence, no
papillary reflex
CL central hemiparesis
Pons

Millard-Gubler syndrome (AS):

Damaged structures in PONS = motor nucleus of CN VII,
corticospinal tract
SS peripheral paresis of facial muscles
CL central hemiparesis
Foville syndrome:
damaged structures = nucleus of CN VI, nucleus of CN VII,
corticospinal tract
SS diplopia, convergent strabismus
SS peripheral paresis of facial muscles
CL central hemiparesis

medulla

Jackson syndrome (AS) = damaged nucleus of CN 12 and

corticospinal tract
SS tongue peripheral paresis

CL central hemiparesis

Lesion of pyramidal system

Level of Damage
Before cervical intermittence (C2-C4)

Spinal cord
(total)

Spinal cord
damage
(partial)

Anterior
horn
Anterior
roots
Peripheral
nerves

Symptoms
Central tetraparesis and
pelvic disorders
nd
Cervical intermittence (2 motor
Mixed tetraparesis =
neuron of upper limbs) = C5-T2
UL peripheral paresis, LL
central paresis
Pelvic disorders
Before Lumbar intermittence, T2-T12 LL central paresis, pelvic
disorders
Lumbar intermittence (L2-S1)
LL peripheral paresis, pelvic
disorders
S2-S5
Pelvic disorders; Impaired
sensitivity of perineum
Brown Sequard syndrome = R or L hemicord lesion
CL disorder of superficial sensation 2-3 segments below lesion
SS movement disorder (corticospinal tract) and deep sensation
disorder (posterior cord). Note corticospinal tract decussates at
medulla so a spinal cord lesion = SS affectation but a lesion above
medulla = CL affectation
SS segmental peripheral paresis without sensitive disorder
(sensation involves posterior horn [superficial] or posterior cord of
spine [deep])
SS segmental peripheral paresis and fasciculations without
sensitive disorder
Peripheral paresis, sensory and autonomic disorders in innervated
areas

Meningeal symptoms
Meningeal symptoms = neck stiffness, Kernigs sign and three brudzinski
Neck stiffness- check by outting ahnd undr neck to judge hwo many figners
are between neck and chest
Kernigs sign- laying down, flex hip and knee; try to extend knee but there is
resistance
+ upper Brudzinksi- flexing neck causing involuntary knee flexion
+middle Brudzinski- pressing on pubic symphysis cause knee flexion
+lower brudzinski- investigating Kernigs sign cause involuntary knee flexion
in other leg

Mengineal pose = head tnrow nback, legs flexed

General hyperesthesia and hypersethsia of sense orgas = photophobia, phonphobia
Reactive painful phenomenon pain when pressing eyeballs, outlet point sof CN 2,5
Electrophysioogical, X rya dn US exam
Electroencephalography- test electrical activity of brain used in epilepsy. Disease
with focal slow activity= encephalitis, tumor, storke brian abscess. EEG can
recognize coma and death
Normal EEG rhythms :
Delta rhythm (<4Hz) in drowsiness, sleep. Abnormal to be seen in awake person
Theta rhythm (4-7 Hz) in drowsiness, sleep. Small amount in an awake person
Alpha (8-13 Hz)when you close eyes and rest
Beta (14-30 Hz) in frontal areas
Pathological patterns= spike and sharp waves (partial epilepsy); generalized waves
= primary generalized epilepsy)
Generalized slowing mostly delta and theta rhythms are seen in metabolic
encephalopahty, post-seizure, dementia, encephalitis, anoxia
Electrocerebal silence = brain death
Evoked potentials, EP- potentials recorded after stimulation
Visual EP- put electrode over occipital lobes and use visual stimulus
brainstem-auditory EP- electrode over vertex and uses auditory stimulus ie click
somatosensory EP - electrode over parietal lobe, stimulate peripheral nerves
Electromyography, EMG- electrical recording of muscle activity. Used for
neuromuscular diseases like muscular dystrophy, myopathies, myotonias,
peripheral neuropathies, radiculopathies, motor neuron diseases like amyotrophic
lateral sclerosis, Gullian Barre syndrome, ataxia, myasthenia. Needle electrode is
inserted into muscle to detect stimulation of muscles by lower motor neuron.
Normal muscle = no EMG at rest or during passive movement
Chronic muscles disorder when muscle fibrous tissue or fat = decreased EMG
Ultrasonogrpahy- use of US
Can detect direction and speed of blood flow. Direction of blood flow changes pitch
of sound wave = Doppler effect. Color flow imaging to visualize vessels, direction of
flow

Signs of brain stem wedge (p.1710=

SS Dilated ppupil
Autonomic disorders = respiratory, cardiac, vadcular tone)
Progressive unconsciousness coma
Encephalitis = inflammation of the brain

Classification
Primary- direct viral infection of brain
Secondary- viral infection at non-brain site but then spreads to brain
Primary = Economo (encephalitis lethargica), tick-born encephalitis, herpetic,
enteroviral
Secondary due to measles, varicella, influenza (these r parainfectious) or
postvaccine
By type of matter affected
White matter= lecuoencephalitis ie HIV, drugs, radiation
Grey matter = polioencephalitis ie poliovirus, coxsackie, enterovirus, rabies
Both white and grey matter = panencephalitis ie herpes, varicella-zoster, HIV, CMV,
measles, syphilis
By etiology:
Viral encephalitis
Bacterial encephalitis
Autoimmune encephalitis
Encephalitis lethargic
Limbic system encephalitis
Syndromes in encephalitis:
-General infectious = fever, fatigue,
-General cerebral = headache, altered mental state, seizures
-Focal
Encephalitic syndrome = paresis/paralysis, hyperkinesis, aphasia, cerebellar
disturbance (different source)
encephalitic symptoms = peripheral paralysis of neck, shoulder and proximal
upper limb = hanging head
**most encephalitis features inflammation and edema (therefore diuretics)
Pathophysiology
Acute encephalitis= inflammation and edema of brain, maybe petechial
hemorrhages if severe. Direct viral infection damages neurons
Acute disseminated encephalitis = inflammation of brain and spinal cord due to
hypersensitive reaction to virus or foreign body
Arbovirus infection, ways of spread
Arbovirus is a term used to refer to a group of viruses that are transmitted by
arthropod vectors.

Arbovirus encephalitis refers to encephalitis that is caused by arbovirus infection.[1]

There are many types of arboviral encephalitides found in the United States.[2]

Examples include:

Tick-borne encephalitis

Japanese encephalitis(mosquito)

California encephalitis

St. Louis encephalitis

West Nile fever (mosquito)

Ways of spread of arboviral infection = bite (transmissive) or by alimentary (ingest

of animal product meat or milk)
Meningeal syndrome in tick borne and influenza encephalitis
Tick-borne or summer-spring encephalitis: B.E.M SYNDROME two fever periods,
meningeal syndrome, encephalitic and bulbar symptoms, general infectious;
paralysis and Kozhevnikov epilepsy
Etiology: neurotrophic tick-borne virus
Carrier of virus= Ixodes tick
Way of spread: bite or alimentary (wild goat milk; multiplication in intestinal
mucosa)
Pathogenesis:
PRIMARY ENCEPHALITIS
virus has trophism to motor structure of brain ie motor nuclei of cranial nerves and
anterior horns of vertical intermittence of cervical spine
Clinic picture: acute and chronic stage
Acute:
fever 40C, fatigue, muscle aches, headache = general infectious signs
meningeal syndrome
brain edema
two fever periods: 1st period for 3-5 days, then 2nd fever
after 2nd fever encephalitic symptoms = peripheral paralysis of neck, shoulder and
proximal upper limb. Characteristic position of hanging head and Paterson cant lift
hands
bulbar symdrome = dysarthria, dysphonia, dysphagia, tongue muscle atrophy
paralytic period of acute phase: increase paresis and atrophy of muscles
Clinical forms of acute stage:
Abortive
Poliomyelitic
Encephalitic
Meningeal
Polyradiucloneuritic
Can recover from acute stage (this takes 2-3 years) or there fi chronic stage

Chronic stage of tick-borne encephalitis:

-Persistent atrophic paresis or paralysis
-Seizures of Kozhevnikov epilepsy = constant myoclonic twitching in certain
muscles, recurrent generalized convulsive seizures
Diagnosis
-epidemiology: hot season i.e. summer, endemic focus of infection, patient had tick
bite
-serology tests for virus
-biological experiment on animals
-typical manifestations = meningeal, encephalitic and bulbar syndromes plus
general infectious.
Treatment
Anti-tick borne immunoglobin, IM
Prednisolone
Ribonuclease to inhibit viral RNA replication, IM
Dehydration tx, Disintoxication tx, maintain electrolyte balance
Symptomatic= anticonvulsants, vitamin therapy
Economo encephalitis or encephalitis lethargic or epidemic encephalitis (Economo
triad, parkinsonism)
-Etiology= unknown virus usually in cold season
-Way of transmission = airborne then virus reaches CNS via blood and lymph from
nasopharynx
Disease leaves people statue-like condition, speechless and motionless
-Pathogenesis :
PRIMARY ENCEPHALITIS
-Clinical picture: acute and chronic
Acute stage: vascular-inflammatory and infiltrative process
Grey matter of hypothalamus, brainstem (CN III nucleus and black substance,
red nucleus,) are affected. Changes are reversible except in substantia nigra
-**Symptoms of acute stage=
Economo triad = oculomotor disorders + fever+ sleep disturbance (sleep in day,
awake at night)
Fever with general cerebral signs = headache , NV
Eye movement disorders: diplopia, ptosis, divergent strabismus, restricted eye
movements, converse Argyll Roberston = pupillary response to light but not no
accommodation. Also weak convergence, look up paresis
Chronic stage:
-Progressing Parkinson syndrome (degenerative change in substantia nigra)
-Vegetative disorders = hypersalivation, hyperhydrosis, greasy face
-Oculomotor disorders: weak convergence, look up paresis. Argyll Robertson with
response to light but not accommodation
Note Argyll Robertson pupil = accommodation but no reaction to light =
neurosyphilis

Parkinson syndrome = lesion in basal ganglia esp substantia nigra

Akinesia or hypokinesia or bradykinesia
Rigidity = hypertone
Static tremor
Parkinsonism = clinical syndrome, tremor, bradykinesia, rigidity, and postural
instability
Causes of Parkinsonism = medications, mainly neuroleptic antipsychotics; toxins,
metabolic disorders
Parkinsons disease = neurodegenerative illness, hereditary usually 45-60 years
Diagnosis of lethargic encephalitis
-inflammatory peripheral blood changes = leukocytosis, increased ESR,
-CSF= clear, mild lymphocytic pleocytosis
Treatment
Acute stage:
Etiotropic tx= interferon,
Pathogenic tx= dehydration, detoxification,
symptomatic methods
Chronic stage= antiParkinson drugs
Levodopa and carbidopa(decarboxylase inhibitor to prevent dopamine breakdown)
Dopamine agonist = bromocriptine
Amantadine to increase sensitivity of dopamine receptors
Anticholinergics
MAO inhibitors to prevent dopamine breakdown

Herpetic encephalitis = most common and severe form of acute encephalitis

Etiology= herpes simplex 1 or 2 which have trophism for ectodermal structure like
skin, CNS, mucosa
Pathogenesis= lesion of temporal and inferior frontal lobe of brain featuring
necrotic foci with hemorrhages b/c virus enters by ophthalmic bulb or trigeminal
ganglion
Clinical picture:
Prodromal period = acute respiratory virus infection with herpetic eruptions on
mucosa
Epileiptic seizures
Focal lesion of temporal and inferior frontal lobe : CN lesions i.e. hemianopsia
Hemiparesis, hyperkinesis, aphasia,
Disturbed smell and hearing, aphasia
Edema brain wedging = respiratory standstill, also bradycardia, hypotension
Diagnosis:

CSF (typical viral changes)= high pressure, lymphocytic pleocytosis, moderate

increase in proteins
PCR = herpes DNA in CSF
CT/MRI =hypodense zones of inflammations, areas of edema and hemorrhage focal
lesions
Treatment
Etiotropic tx = Acyclovir to inhibit viral DNA synthesis
Dehydration tx= osmotic diruteics ie mannitol, lasix
Symptomatic tx
Enteroviral encephalitis
Etiology: enterovirus = coxsackie , ECHO
Pathogenesis:
PRIMARY ENCEPHALITIS
perivascular edema in cortex, focal destruction of white substance, vascular
inflammatory changes
Clinical picture:
General infectious
General cerebral
Focal signs: paresis , paralysis , aphasia,
CN lesion i.e. CN 3 and 8 (hearing loss), bulbar syndrome, cerebellar syndrome
Diagnosis
Appearance of focal symptoms 2-5 days after upper respiratory disorders or
subferbile temp and general weakness
CSF= increased pressure and lymphocytic pleocytosis
Treatment
Pathogenetic = detoxification
Symptomatic
Influenza encephalitis
Etiology: influenza virus A1,2,3 and B
Pathogenesis : SECONDARY ENCEPHALITIS
Virus has toxic affect on brain vessels neurotoxicosis and circulatory disturbance
Clinical pic:
General cerebral, meningeal and focal symptoms after the flu
General weakness, irritability
Psychotic disorders i.e. hallucinations, delirium, seizures
CN lesion of CN 3,4,6,7,12 and pyramidal tract
*hemorrhage can develop in toxic form
CSF (typical of virus) = lymphocytic pleocytosis, increased protein, blood trace
Treatment of flu encephalitis
Disintoxication
Diuretics

Gamma globulin
Rheumatic encephalitis
Etiology: during rheumatism (Group A beta-haemolytic Streptococcus) CNS can be
involved. Forms = acute rheumatic meningoencephaltis, small chorea
Pathology: affected cerebral cortex, subcortical structures, brainstem and meninges.
Vascular changes in brain i.e. endarteritis, vasculitis,
Small chorea = rheumatism with damage to subcortical nodes
Signs= general cerebral signs, choreic hyperkinesis = fast involuntary chaotic
movements in muscles
Diagnosis:
If rheumatism is present i.e. rheumatic carditis, rhematuic nodules in joints
Treatment
For rheumatism (staphylococcus)= penicillin
Sedative tx for hyperkinesis
Post vaccine encephalitis
Etiology= develops after vaccine ie anti-rabies, antidiphtheritic
Pathogenesis: small hemorrhage, brain edema, focal demyelinization
Clinical features:
Develops 7 or more days after vaccine with increased temperature 39C, headache ,
vomiting, impaired consciousness, seizures = general cerebral
May see meningeal syndrome
May see paresis, paralysis, coordination disorders
*Rabies reaction gives encephalomyelopolyradiculoneuritis with bulbar syndrome
with disturbed breathing and cardiovascular activity which can be lethal
Treatment:
Desensibilization (loratadine, tavegil, suprastin)
Diuretics
Antiseizure medication
antipyretics

Myelitis inflammation of spinal cord

Etiology:
Viral i.e. enterovirus, herpes
Bacterial ie treponema pallidum, MBT
Fungi and protista rare
Usually in lower thoracic spine
Clinical features

-General inflammation signs with mild fever

-Intense pain at level of destruction, then paresis of lower trunk and limbs,
conductive sensitivity disorders and pelvic disorders
CSF change based on if viral or bacterial
To ddx, spinal stroke from myelitis : spinal stroke has no general inflammatory
changes, no changes in CSF, preserved deep sensitivity
?To ddx myelitis from Gullian Barre; babskinski symptoms, conductivity disorders
and pelvic disorders in myelitis
Treatment
Etiologix tx whether viral, TB, bacterial
Prednisolone:
Antibiotics to prevent superinfection
Bladder care
Acute Poliomyelitis
Etiology= poliovirus
Pathogenesis:
Poliovirus targets anterior horn of spinal cord and brainstem motor nuclei
Clinical picture:
Incubation 10-14 days
Clinical forms of acute poliomyelitis
Asymptomatic form 95%
Abortive from= self limiting to GI and respiratory system with pyrexia
Non paralytic from = meningism and abortive poliomyelitis (respiratory
system with pyrexia)
Meningism = neck stiffness, photophobia, headache; irritation of meninges without
actually infection or inflammation
Paralytic poliomyelitis form:
Prodromal = fever, myalgia, meningism, GI disorder
Preparalytic stage: spasms, change of muscle tone,
Paralytic = asymmetric peripheral paralysis usu in lower limbs. Can be respiratory
failure due to muscle paralysis
?Ddx acute poliomyelitis from Gullian Barre: poliomyelitis has asymmetry and lack
of sensory disorder
Treatment
Immungolbulin IM
Antibiotics for pneumonia prophylaxis
Pshyiotherapy
Neurosyphilis
Etiology= trepnomea pallidum (spirochete)
Pathogenesis=

3 stages
Primary 10-30 days or 2-3 weeks after infection = chancre
Secondary= 6 weeks-6 months later, with eruption/rash = painless, non itching
papules
Tertiary stage = 10-20 years later, CNS involvement
CSF changes (typical of viral)=
aseptic inflammation
lymphocytic pleocytosis
protein
glucose
+ serological test for syphilis = + Wasserman or PCR to detect treponema DNA
from CSF or
Symptoms in neurosyphilis
Optic atrophy = direct Argyll Robertson syndrome = accommodation but no
light pupillary reaction with unequal pupils
Paralysis due to UMN lesion; Acute hemiplegia (small arteries become
inflamed and obliterated) and individual CN palsies
Loss of proprioception in legs = wide stomping gait
Clinical forms:
Early mesodermal syphilis
1. Asymptomatic neurosyphilis
2. Acute syphilitic meningitis = severe headache, meningeal syndrome.
Localization of base of brain = affected CN 2, 3-6 ; direct Argyll Robertson
pupil; maybe anioscoria, pupil deformation,, CSF changes listed above
3. Chronic basal syphilitic meningitis subacute onset;
General cerebral and meningeal symptoms
CN lesion:
Atrophy of CN 2
CN 3 = ptosis, diplopia
peripheral palsy of CN 7
Disorders of CN 8
4. Meningovascular syphilis features obliterative inflammation of vessels
brain and spinal cord infarction
General cerebral, meningeal and focal signs (CN III disorder in one eye with
direct Argyll Robertson syndrome
5. Gummy brain and spinal cord individual focal lesion in brain aka a
granuloma
Similar presentation to a tumor = protein-cell dissociation in CSF
Usually localized in fossa interpeduncularis
Hypertensive syndrome = headache, vomiting, papilloedema
Focal signs = paralysis, sensory disorders, aphasia, agnosia
Late ectodermal or parenchymatous neurosyphilis.
1. Progressive paralysis- memory disturbances. loss of acquired skills= disorders
of speech, writing and reading

2. Tabes dorsalis
3. Taboparalysis tabes dorsalis and progressive paralysis
Tabes dorsalis- degeneration of posterior columns and posterior roots, some CN
lesions (2,3,5,8)
3 stages: neuralgic, ataxic, paralytic
Neuralgic- paraesthesia usu severe, sudden pain; visceral crisis = attack
neurological pain in internal organs ie stomach, intestinal, heart, liver, kidney,
bladder crisis.
Specific sign = direct Argyll Robertson syndrome, anisocoria
Focal lesion: CN2 atrophy, CN 3, CN 5 trigeminal neuralgia, CN 8
Ataxic- coordination disorders and unstable walking and standing due to
damage of posterior funiculus
Paralytic stage severe motor dysfunction, loss of afferentation, trophic and
pelvic disorders
Diagnosis of neurosyphylis
+ Wasserman blood and CSF ; immobilization of treponema
PCR= treponema DNA in CSF
Immunefluorescent assay to detect treponema in blood and CSF
Treatment
Early syphilis = penicillin
Check CSF exam with lumbar puncture
Neuroborrelosis (lyme disease)
Causative agent = Borrelia burgdorfei (spirochete)
Carrier tick = Ixodes
Clinical picture=
stage 1 = 3-30 days after the bite, relapsing remitting pyrexia and arthalgia with
skin lesion of erthyema cornicum migrans at bite site
stage 2 few weeks or months after stage 1 = cardiac symptoms or neurological
symptoms ie CN affection ie. unilateral/bilateral CN 7 palsy, peripheral neuropathy
Stage 3 occurs after months and years = recurrent, erosive arthritis can also have
seizures, behavioral disorders
Diagnosis of Lyme disease
Clinical picture and epidemiology
Serological and PCR methods
Treatment of Lyme disease
Antibiotics orally i.e. penicillin, tetracycline and IV penicillin, ceftriaxone

HIV associated nervous system disorder

Causative agent = HIV,a retrovirus

Transmission = sexual, parenteral (needles, bllod trnafusion), vertical from mom to

baby
HIV affects CD4+ lymphocytes
HIV can affect neural structure directly, by blood or perineurally
Classification:
Primary- HIV affects nervous system directly
Secondary- opportunistic infections and tumors due to immunodeficiency
Primary HIV Nervous system disorder
HIV associated dementia
Aseptic meningitis
Vascular neuroAIDS
HIV associated neuropathies : Gullian-Barre syndrome
Secondary HIV Nervous system disorder
Toxoplasmotic encephalitis
Herpetic encephalitis
CMV encephalitis
Crytococcal encephalitis
CNS lymphoma dn Kaposi sarcoma
Progressive mutlifocla leukoencephalopahty
HIV encephalopathy
-Morphological unit = primary lesion of white matter of cerebral hemisphere that is
inflammatory and demyelinating
-Signs: behavioral changes, cognitive changes (slowed intellect), movement
disorders (ie ataxia, central pareis, hyperkinesis); tremor , seizures
-Diagnosis
CT/MRI= cortical atrophy with widened subarachnoid spaces and ventricles
CSF= slight lymphocytic pleocytois, modeate increa ein proteins, high HIV antibody
titre
HIV aseptic meningitis
General infectious, meningeal syndromes with and CSF changes
HIV associated vascular meylopathy
Demyeliantion and degenaraton of spinal cord in lateral and psoterir funcilcui in
thoracic psine
Senstitive ataxia, conducitve sensitive disorders, paraparesis, pelvic disoerders
MRI = atrophy of spine
Vascular neuro AIDS
Virus induced vasculitis of brain and spinal cord thrombosis and infarction
Clinical pic= TIA, then ischemic stroke. Repeated ischemic stroke = focal lesions ie
paresis, ataxia, etc
Hemorrhagic stroke possible
Treatment of primary AIDS

HAART therapy = highly active antiretroviral therapy to inhibit the disease

progression of 2 groups
Inhibits HIV enzyme revertase i.e. zidovudine,
Inhibits viral enzyme protease i.e. indinavir, ritovir
SECONDARY HIV ASSOCIATED DISEASES
Progressive multifocal leuko encephalopahty
Demyelinating disease caused by papovavirus JC during immunosupression
-Signs : dementia, headache, progressive paresis, sensory diseases, seizures
-Diagnosis :
PCR finds JC genetic matter
CT/MRI = multiple foci of low density in white matter.
Toxoplasmatic encephalitis
-most common cause of lesion in AIDS patient
Focal neurological symptoms = aphasia, CN lesion, hemiparesis, sensory and motor
disorders
Cerebal symtopms = headhache, confusion
Eye lesion occur before or with CNS lesion ie uvetiis, papilltiis
-Diagnosis:
PCR= toxoplasmosis DNA in blood, CSF
CT/MRI ring shape dfoci wth peripheral swelling usu in fortnal-parietal areas
Treatment = pyrimethamine and sulfadiazine or clindamycin
Crytoptococcal encephalitis
General cerebral signs = headache, nausea, impaired consciousness, eizures
General infections signs-= weight loss, fever
Fical signs: CN lesions,
Somatic manifestations: pneumonia, urinary bladders infection, skin lesions
Treatment= amphotericin B, itraconazole
Neoplasms
Intracranial hypertension
Symptoms: confusion, memory and behavioral change, CN lesions, hemiparesis,
seizures
CT/MRI= mass
Fundoscopy= papilloedema
Brain abscess
https://en.wikipedia.org/wiki/Mass_effect_%28medicine%29
http://radiopaedia.org/articles/epidural-empyema
http://emedicine.medscape.com/article/1168415-overview ,
http://radiopaedia.org/articles/subdural-empyema subdural empyema

https://en.wikipedia.org/wiki/Creutzfeldt%E2%80%93Jakob_disease
https://en.wikipedia.org/wiki/Parkinsonism
http://www.movementdisorders.org/MDS/About/Movement-DisorderOverviews/Parkinsons-Disease--Parkinsonism.htm
http://www.fpnotebook.com/eye/Pupil/ArgylRbrtsnPpl.htm Argyll Rorbertson
http://lifeinthefastlane.com/ophthalmology-befuddler-017/
http://www.sturge-weber.org/medical-matters/types-of-seizures.html