applied neurosciences

Applied NeurosciencesDone by:

Ahmed Khalafalla MohammedAhmed Abdalla Alamin

Topics

Sensory System.Special senses:

◦Eye.◦Ear.

Motor System.Cranial nerves.Nerve conduction

study.EEG.Neuro-microbiology.

Imaging.Neurology.Neuro-surgery.

Sensory System

Lesion affecting the spinothalamic tract only; Syringomyelia:

Signs: Dissociated sensory loss of the affected segment;◦Loss of pain & temperature.◦Intact touch (fine touch).◦Intact motor function.

Sensory System

Lesion affecting the spinothalamic tract with concomitant motor impairment; Anterior cord syndrome:

Signs of the affected segment;◦Loss of pain & temperature.◦Intact touch (fine touch).◦Loss of motor function.

Sensory System

Lesion affecting the dorsal column tract only;

Seen in posterior cord syndrome, 3ry syphilis (Tabes dorsalis) etc…

Signs of the affected segment; sensory ataxia:◦Loss of vibratory & positional sense. +ve Romberg sign.

◦Intact pain & temperature.◦Intact motor function.

Sensory System

Lesions affecting both tracts; the spinothalamic & the dorsal column tracts: lesions affecting one side of the spine (e.g. Brown-Sequerd syndrome):

Ipsilateral loss of fine (complex) touch, pressure, vibration, position sense & two points discrimination sensations. Impaired motor function.

Contralateral loss of crude (simple) touch, temperature, pain, sexual and itching sensations. Intact motor function.

Sensory System

Lesions affecting both tracts; the spinothalamic & the dorsal column tract: lesions affecting both sides of the spine (e.g. cord transection):

Bilateral loss of all sensations at and below the level of the lesion. Impaired motor function.

Sensory System

Lesions affecting both tracts; the spinothalamic & the dorsal column tracts: lesions affecting the thalamus:

One thalamus: contralateral loss of sensation but the pt still can smell.

Both thalami: impaired sensation sparing the ability to smell.

Sensory System

Lesions affecting the somatosensory cortex:Primary SC (areas 3,1,2): contralateral

impaired sensation but the pt still can feel the pain (by the thalamus) but he can’t localize it.

S association C (areas 5,7): tactile agnosia; difficulty in recognizing, naming & memorizing objects placed on one hand while eyes are closed.

Eye

Light reflex:Direct on the examined eye.Indirect (consensual) on the other one.Abnormalities:

◦Bilaterally: Argyll Robertson pupil; impaired light reflex with intact accommodation. Caused by syphilis.

◦Unilaterally: Holmes-Adie (myotonic) pupil; impaired light reflex with sluggish accommodation.

Eye

Fundoscopy (Ophthalmoscopy):For examination of the retina (macula,

optic disc and blood vessels).For detection of Papilledema (swelling of

the optic disc) which indicates increased ICP so lumbar puncture will be contraindicated.

Eye

Ophthalmoscopes:

Eye

Ophthalmoscopy:

Eye

Retina:

Eye

Visual Acuity:Snellen’s

charts are used.

Normal ratio is 6/6.

Eye

Color vision:Ishihara charts are used for examination.Color blindness is X-linked so male are

more prone to get it.

Eye

Ishihara charts:

Eye

Visual Field:Using no machines; confrontation method.Using special machines; Perimetry.

Eye

Goldmann kinetic Perimeter

Eye

Automated Perimetry:

Ear

Weber’s test.Rinne’s test.

Tunning Fork

Ear

Weber’s test:Normally; pt hears

equally on both sides.Conductive deafness;

pt hears better on the affected side (due to loss of masking effect of the environment).

Nerve deafness; pt hears better on the normal side.

Ear

Rinne’s test:Normally; air conduction is

better than bone conduction.

Conductive deafness; pt hears bone conduction but not the air conduction.

Nerve deafness; pt does not hear any sound whether it is through bone or air conduction.

Ear

Audiometery:Audiometer is used.It presents tone with

different intensities and frequencies to a pt through earphones.

Audible frequencies are plotted against intensities on a graph paper. It is called audiogram.

Ear

Normal Patient

Ear

Conductive deafness

Ear

Nerve deafness

Ear

Mixed deafness

Motor System

Examination of deep reflexes:Based on the stretch reflex.The “Hammer” is used.Hyper-reflexia in UMNL.Hypo-reflexia in LMNL.

Motor System

Knee reflex; (L1,2,3 ).Biceps reflex; (C5,6).Ankle reflex; (S1).

Motor System

Lesions affecting the pyramidal system:At the cortex → contralateral flaccid weakness that is

limited to a particular area (e.g. monoparesis). At the internal capsule → contralateral paralysis or

weakness (hemiplegia). At the brain stem → contralateral paralysis or

weakness (hemiplegia) + ipsilateral cranial nerve palsy.At the spinal cord:

◦Complete transection → quadriplegia (cervical lesion below C4) or paraplegia (thoracic lesion).

◦Hemisection → ipsilateral hemiplegia (cervical lesion below C4) or ipsilateral monoplegia (thoracic lesion).

Motor System

Lesions affecting the extra-pyramidal system:

At the basal ganglia.At the cerebellum.

Motor System

Disorders of the basal ganglia: Hyperkinetic disorders; Tics, Chorea,

Athetosis, Ballismus and Dystonia. Hypokinetic disorders; Parkinson’s

disease.

Motor System

Tics:Repeated

involuntary movements.

Mostly in the face.

Motor System

Chorea:Dancing movement.Impaired caudate

nucleas.

Motor System

Athetosis:Slow writhing, pronounced in hands, fingers

and may be in the neck.

Motor System

Balismus:Violent movement in

one side of the body (hemi-balismaus).

Motor System

Parkinson’s Disease:

Resting tremor.Slow shuffling gate.Akinesia. Bradykinesia.

Motor System

Lesions affecting the cerebellum:Cerebellar ataxia:•Delay in movement initiation.•Dysmetria: alterations in the rate and force of a movement. •Asynergia: decomposition of movement. •Past Pointing. •Intention Tremor. •Dysarthria. •Dysdiadochokinesis. •hypotonia.

Motor system

Nystagmus is involuntary rhythmic movement of the eyes consisting of slow movement in one direction (due pathology of ocular muscles) and rapid/fast return movement in the other (due to pontine stimulation, this movement determines the direction of nystagmus).

Nystagmus increases when the patient gazes in the direction of the fast component.

Motor System

Motor System

Heel to toe walking :Impaired when

vestibulocerebellum is impaired

Archicerebellar Syndrome

Heel to shin & Fast repetitive movements:

Impaired when cerebrocerebellum is impaired

Neocerebellar Syndrome

Motor System

Romberg test:Ask the pt to stand with close

feet while eyes are open and then he closes his eyes & you note his balance. Also +ve in lesions affecting the dorsal column.

Finger-Nose test:Ask the pt to touch your finger

tip & then he touches the tip of his nose repeatedly while you are moving your hand.

Cranial Nerves

Olfactory Nerve lesion; Anosmia.

Cranial Nerves

Optic nerve:

Right nasal hemianopiaLoss of right eye visionBitemporal heteronymus hemianopia

Left homonymus hemianopiawith macular sparing

(NB: the macula has a duel blood supply.)

Cranial Nerves

Oculomotor nerve:Ptosis.Able to abduct his

eye.According to the

impaired part of the nerve, ocular motor deficit occurs.

Cranial Nerve

Trochlear nerve:Eye is upward and

medially rotated due to un opposed action of the SR muscle.

Impaired abduction.

Paralyzed SO muscle.

Cranial nerves

Trigeminal nerve:Numb face.Atrophied muscles of

mastication.

Cranial Nerves

Abducent nerve:Eye is medially

rotated due to unopposed action of MR.

Impaired abduction of the affected eye.

Cranial Nerves

Facial nerve:Upper part of the face receives duel motor supply

from both cerebral hemispheres.Lower part of the face receives single motor supply

from the contralateral cerebral hemisphere.UMNL; Contralateral paralysis of the lower half of the

face + Contralateral hemiplegia (Nb: hemiplegia is ipsilateral to the paralyzed site of the face & contralateral to the lesion site).

LMNL at the level of pons; Ipsilateral paralysis of half of the face (upper & lower) + Contralateral hemiplegia.

LMNL at the nerve level; Ipsilateral paralysis of half of the face only.

Cranial Nerves

UMNLLMNL (e.g. bell’s palsy)

Cranial Nerves

Vestibulo-cochlear nerve:Vestibular nerve; vertigo (not as fainting).Cochlear nerve; deafness.

Cranial Nerves

Glossopharyngeal and vagus nerves:Gag reflex (for both). Unilateral vagus lesion; deviated uvula to

the opposite site.Bilateral vagus lesion; uvula does not lift.

Cranial Nerves

Accessory nerve:Bilaterally; ask the pt to flex his neck and

resist the movement.Unilaterally; ask the pt to turn his head to

one side and resist him.Ask the to shrug his shoulder.

Cranial Nerve

Hypoglossal nerve:Ask the pt to put out his tongue:

◦UMNL; tongue deviates to the side opposite to the lesion.

◦LMNL; tongue deviates to the same side of the lesion, fasciculation & atrophy.

Cranial Nerves

Test:

Nerve Conduction Studies

They are:1. Sensory studies : nerves are studied by

stimulating them at one point and recording at a distant site along those nerves.

2. Motor studies : nerves are studied by stimulating them at two points (proximal + distal) and recording the muscle action potentials or stimulating them at one point & recording them at two points.


Parameters for nerve studies:1. Amplitude → reduced due axonal neuropathy e.g.

Diabetic axonal neuropathy.2. Velocity (can be calculated from both distance

between the cathodes and latency period between stimulation and wave appearance) → slow in demyelination neuropathy (e.g. Guillian-Barré syndrome).

• These parameters are normal in Myasthenia gravis.• Both parameters are found defective in severe cases

of local nerve entrapment (e.g. Carpel tunnel syndrome).


Sensory studies:1. Amplitude (10 µV)2. Velocity (70-90 m/s)


Recording electrodes

Stimulating electrodes


Motor studies: 1. Amplitude (2-3 mV).2. Velocity (50-70 m/s).


Recording electrodes

Stimulating electrode

EEG

The Electro-Encephalo-Gram:It is a record of the electrical

activity of the brain using electrodes placed on the scalp or directly on the surface of the cortex.

It can be unipolar or bipolar.

EEG

EpilepsyEpilepsy is a chronic brain disorder

characterized by recurrent synchronous discharges of neuronal groups in the cortex.

The discharges, which are also called seizures, may be localized or generalized.

Seizures have been classified as partial or generalized, depending on the spread, and medication is selected on the basis of the classification.

EEG

Classification of epilepsy:Partial; simple or complex.Generalized;

◦Tonic clonic (grand mal) seizures.◦Absence (petit mal) seizures.◦Other types; myoclonic, febrile & status

epilepticus.

EEG

In generalized, or non-focal, seizures, there is a massive spread of electrical activity over both hemispheres.

Petit mal (absence) seizures, which begin in childhood, involve a transient loss of consciousness without a loss of muscle tone, so those patients rarely fall down.

In grand mal (tonic-clonic) seizures, the patient suddenly loses consciousness and falls down. Convulsions consist of increased muscle tone (tonic) periods alternating with jerking movements (clonic). After the convulsions, loss of consciousness may persist.

Status epilepticus is a dangerous, uninterrupted series of seizures that requires urgent intravenous administration of drugs.

EEG

Partial (focal) seizures result from localized discharges that spread from the focus to adjacent brain areas. The patient may remain conscious, and the nature of the seizure depends on the area of the brain affected. Discharges in the motor cortex may involve first the seemingly purposeful movement of extremities (fingers), with spread up the arms to the face, and down to the legs as neuronal groups are progressively recruited into the discharge.

Motor seizures are also called jacksonian motor seizures. In simple partial seizures, the patient remains

conscious, but if activity spreads to the other hemisphere, the patient may lose consciousness and the seizure is termed complex or psychomotor, since there may be hallucinatory experiences.

EEG

On EEGA focal seizure produces a characteristic EEG

spike, whereas a generalized seizure produces a series of spikes that are picked up all over the skull simultaneously. The EEG also distinguishes between the tonic and clonic phases of the generalized discharge.

During absence seizures, there are characteristic spike & wave patterns of discharge.

EEG

Treatment; anti-epileptics:Partial and grand mal seizures; Na

valproate, phenytoin & carbamazepine.For pregnant ladies; lamotrigineAbsent seizures; ethosuximide.Status epilepticus; emergency tx:

lorazepam, diazepam.

Neuro-Microbiology

Medically important microbial diseases of the Nervous System:

Meningitis.Encephalitis.Brain abscess.Pott’s disease.Botulism.Tetanus.Poliomyelitis.Rabies.AIDS opportunistic infections.Sleeping sickness.Post infection Guillian-Barré syndrome.

Neuro-Microbiology

Meningitis:Inflammation of the meninges which it is

characterized by headache, fever, neck stiffness, photophobia, rash (meningococcal rash), etc..

Forms: ◦Acute meningitis.◦Chronic meningitis.

Neuro-Microbiology

Acute meningitis:Pyogenic (usually bacterial); which is

generally caused by:◦S. pneumoniae, N. menigitidis & H. influenzae

cause meningitis in childern.◦E. coli & S. agalactae cause neonatal meningitis.◦S. pneumoniae, N. menigitidis & L. monocytogenes

cause meningitis in adults.Aseptic (usually viral); caused by

enteroviruses, mumps, HSV-2, varicella-zoster virus, HIV, Epstein-Barr virus, LCMV, etc...

Neuro-Microbiology

Chronic meningitis:Tuberculous meningitis.Meningiovascular syphilis.Lyme disease.Cryptococcus neoformans.

Neuro-Microbiology

Causative agent

WBCs Differential RBCs Protein Glucose

Bacterial >200/µl Polymorphs Few High Low

Viral <200/µl Lymphocytes - Slight high

Normal

Fungal <50/µl Lymphocytes - Not high Low

TB 50-500/µl Lymphocytes - usually Low

Typical changes in the CSF in different types of meningitis

Neuro-Microbiology

Encephalitis:Infection of the brain parenchyma.Characterized by; headache, fever, personality

change, hallucinations, aphasia, signs of meningism.

Caused by:◦Bacterial; bartonella, mycoplasma, listeria.◦Parasitic; malaria, toxoplasma, sleeping sickness,

naegleria.◦Viral (commonest); HSV (most common cause, Mx:

acyclovir), enteroviruses, rabies, paramyxoviruses, arboviruses, CMV.

Neuro-Microbiology

Post infectious encephalitis:Following viral infection:

◦Measles.◦Mumps.◦Rubella.◦VZV.

Diagnosis of encephalitis; PCR for viral genome, MRI.

Neuro-Microbiology

CNS abscesses:Focal pyogenic infection.Exerted effects by:

◦Brain/spine damage.◦Paranchymal compression.◦Raised ICP.◦ Interfering with blood/CSF flow.

Include:◦Brain abscess.◦Subdural empyema.◦Intracranial epidural abscess.◦Spinal epidural abscess.◦Spinal cord abscesses.

Neuro-Microbiology

Brain abscess:Often polymicrobial (strep., enteric, anaerobes);

S. aureus may causes abscess associated with IE.Less common etiologies; nocardia, fungi, T. gondii

& neurocystocercosis.Clinical features; headache, fever, mental status

changes, hemiparesis, papilledema.Diagnosis; neuroimaging, lumbar puncture is

contraindicted.Treatment; surgico-medical, prophlyctic

antiepileptic agents, measures to lower ICP.

Neuro-Microbiology

Ring-shaped enhancement following contrast administration on CT (Abscess):

Neuro-Microbiology

Pott’s disease:Often preceded by pulmonary TB. It attacks

the vertebral bodies of the spinal column making kyphosis.

Charachterized by; signs and symptoms of TB (e.g. night sweating), back pain, weakness.

Diagnosis; imaging of the chest for former TB infection, spinal MRI, PCR, ELISA, culture.

Treatment; TB regimen.

Neuro-Microbiology

Guillian-Barré syndrome:Immuno-mediated acute inflammatory demyelinating

polyneuropathy. Characterized by progressive weakness & areflexia.

Differential diagnosis can be mixed with polio (acute flaccid paralysis) but the incidence of polio is low.

Associated infections:◦ Viral; inflenza, EBV, HSV, CMV, HIV, WestNV.◦ Bacterial; C. jejuni, Mycoplasma.◦ Parasitic; malaria (P. falciparum).◦ Vaccination; inflenza (swine).

Diagnosis; typical clinical features, high CSF protein, recovering from febrile illness, immuno-diagnosis.

Treatment; plasmapharesis, immunoglobulins.

Neuro-Microbiology

AIDS opportunistic infections:Many causative agents but mainly:

◦Toxoplasmosis; cause focal calcified or ring enhancing masses lesions with focal neurological symptoms.

◦CMV; cause encephalitis, myelitis, treated with ganciclovir.

◦Cryptococcal meningitis.◦JC virus; cause progressive multifocal

leucoencephalopathy.

Imaging

Imaging modalities of the CNS:Spiral Computed Tomography scanning (CT)

for brain imaging mainly (it is the primary modality). It can be used in spinal imaging in certain cases & when MRI is contraindicated.

Magnetic Resonance Imaging (MRI) for brain and spinal imaging.

Ultrasonograghy is used for infants by placing the probe on the fontanels before they close.

X rays are used also.

Imaging

CT MRI

Quicker. CT scan is superior in head

trauma.CT measures densities.Bright = Hyperdense.Black = Hypodense.Bone is hyperdense.CSF & water are hypodense.Axial (horizontal) images

only.

Slow.MRI is superior in detecting

strokes.MRI measures signal

intensities.Bright = hyperintenseBlack = hypointense.Bone is hypointense.CSF & water are hyperintense

in T2 & hypointense in T1.Multi-axial images.

Imaging

Type of hemorrhage

Time course Mass effect

Acute ≈ 8 to 72 hrs +++

Early subacute ≈ 3 days to 1 wk +++/++

Late subacute ≈ 1 wk to months ±

Chronic Months to years ــ

Imaging

CT:It is primary modality of brain imaging even

though it is not as sensitive as the MRI in detecting strokes. That is because it very quick & shows blood & other secondary causes of strokes.

With or without contrast.Bone and calcifications are hyperdense.Acute hemorrhage is hyperdense.Early sub-acute hemorrhage is hyperdense. Late sub-acute hemorrhage is isodense to brain.Chronic hemorrhage is hypodense.Infarcts are hypodense.

Imaging

Spiral CT machine

Imaging CT images showing base of the skull

Imaging CT images showing pons & cerebellum

Imaging CT images showing the midbrain

Imaging CT images showing Lateral ventricles

Imaging CT with contrast images showing circle of Willis

Imaging

MRITwo major types of images.

◦T1-wighted images.◦T2-wighted images.

Imaging

T1W images T2W images With or without contrast

(gadolinium) CSF & water are hypointense. Bone and calcifications are

hypointense. Acute hemmorrhage is

iso/hypo-intense. Subacute hemmorrhage is

hyperintense. Chronic hemmorrhage is

hypointense. Infarcts are hypointense in

general.

Without contrast. CSF & water are hyperintense. Bone and calcifications are

hypointense. Acute hemmorrhage is

hypointense. Early subacute hemmorrhage

is hypointense. Late SH is hyperintense + low signal.

Chronic hemmorrhage is hypointense.

Infarcts are hyperintense in general.

Imaging

T2-weighted imageT1-weighted image

Imaging

Neurology

Stroke.Myasthenia Gravis.

Neurology

StrokeTwo types:1. Ischemic. 2. Hemorrhagic.

They are not distinguishable clinically but there are pointers;

◦ Hemorrhage (meningism, severe headache & coma) .◦ Ischemia (carotid bruit, Atrial fibrillation, past TIA,

IHD).

Neurology

Causes of cerebrovascular diseases:Infarction – 71 - 85%Hemorrhage (intracerebral) – 10 - 26%Others (CST, SAH) – 2.9 - 5%

Neurology

Risk factors for Stroke:Hypertension; remains the main modifiable

risk factor for stroke.Diabetes Mellitus.Hypercholesterolemia, IHD.Sickle cell disease.SmokingPhysical inactivity, Obesity & alcohol.TIA.Others.

Neurology

On Examination:Atrial fibrillation (AF) - emboli.Heart valve disease – cardio-embolic

stroke.Carotid bruits are not predictive of

severity of carotid stenosis.Cerebral bruits may suggest arterio-

venous malformation.

Neurology

Transient ischemic attack (TIA or Mini Stroke): TIA is a very small stroke that is caused by a temporary

blocked blood vessel and leaves no permanent brain damage.

A TIA is a warning that there is something seriously wrong with the blood flow to the brain and that the individual is at risk of having a full-blown stroke.

Most symptoms of a TIA disappear within an hour, although they may persist for up to 24 hours.

About one-third of those who have a TIA will have an acute stroke sometime in the future. 5-10 times risk of subsequent stroke.

As many as 20% may sustain a small infarct visible on CT.

Only 15% of strokes are preceded by TIAs.

Neurology

Neurology

ACA territory infarct on CT

Neurology

ACA territory infarct on MRI

Neurology

MCA territory infarct on CT

Neurology MCA territory infarct With occluded MCA on CT

Neurology

MCA territory infarct on MR

Neurology

PCA territory infarct on CT

Neurology

PCA territory infarct on MRI

Neurology Young infarct on MR

Neurology

Intra-cerebral hemorrhage

Note the fluid/fluid level between CSF (up) & blood

(below) by the effect of gravity

Neurology

Subarachnoid hemorrhage: It is spontaneous bleeding into the subarachnoid space. Caused by; rupture of aneurysms, arterio-venous

malformations, etc.. Symptoms & signs:

◦ Sudden acute ‘worst ever’ headache which is often occipital.◦ Neck stiffness due to meningeal irritation that should

differentiated from meningitis.◦ Vomiting, collapse, seizures and coma may follow.

Diagnosis; finding blood stained CSF in lumbar puncture & on CT.

Management; supportive, surgery, etc.. Complications; rebleeding, ischemia, hydrocephalus,

hyponatermia.

Neurology

CT image shows Subarachnoid hemorrhage

NB: The presence of CSF/blood mixture makes CSF hyperdense

Neurology

Myasthenia Gravis:It is a disorder of the neuromuscular

transmission characterized by variable muscle weakness (hypotonic) and fatiguing that is relieved by rest.

Caused by; an organ-specific autoimmune reaction with antibodies directed against acetylcholine receptors (nicotinic receptors).

Neurology

Clinical features:Up to 90% of pts present in early adult life (<40

yrs of age).Women are more affected.Several clinical subdivisions:

◦Grade I; Ocular manifestation. 40% become Gd II.◦Grade IIA; Mild generalized weakness.◦Grade IIB; Moderate generalized weakness.◦Grade III; Acute fulminating.◦Grade IV; severe upon mild or moderate at onset.

Grades IIB, III & IV develop respiratory muscle involvement.

Neurology

Sign and symptoms:Of cranial nerves:

◦Ptosis, ocular muscle paresis.◦Mouth is hanging open.◦Expressionless face.

Of limb and trunk:◦Lolling of the head (neck weakness).◦Proximal limbs are preferentially affected.◦Stress, infection and pregnancy all exacerbate

the weakness.

Neurology

Investigations:Pharmacological; edrophonium test.Serological; anti-acetylcholine receptors

Abs.EMG; reduced amplitude of the compound

muscle action potential.Additional; pt with thymoma may need X-

ray or CT images.

Neurology

Treatment:Symptomatic; cholinesterase inhibitors.Immune; immune suppression, plasma

pharesis and even thymectomy.Supportive; NGT, ventilation, etcDrugs to avoid; that cause or precipitate

myasthenic crisis and repress respiration, beta blockers, Ca channels blockers, amino-glycosides, erythromycin, etc..

Neurology

Other forms of Myasthenias:Neonatal myasthenia:

◦Born to mothers with MG.◦Due to autoimmune Abs (IgG) attacking NMJ.◦Starts within 48 hrs & ends 2-12 wks.

Congenital myasthenia:◦Non-autoimmune.◦Due to structural abnormalities of the receptors

themselves caused by gene mutations.◦Does not respond well to MG treatment.

Neuro-Surgery

Head injury.Raised intracranial pressure.Hydrocephalus.

Neuro-Surgery

Head injury:Brain damage may occur from primary

injury or the secondary effects of that injury.

Neuro-Surgery

Primary brain damage:Cortical contusion and lacerations; occur

under the site of the injury or opposite (contre-coup)it.

Diffuse white matter lesions; as a result of shearing following deceleration and damaging the axons.

Neuro-Surgery

Secondary brain damage:Hemorrhage:

◦Epidural (extradural) hematoma.◦Subdural hemorrhage.

Brain swelling (edema).Brain shift & tentorial/tonsillar herniation.Ischemia.Infection.

Neuro-Surgery

Examination:Lacerations and bruising; indicate the presence of

fractures.Basal skull fracture signs.Conscious level; Glasgow coma scale.Pupil reflex; tests optic & oculomotor nerves but

the latter is important regarding herniations & expanding masses.

Limb weakness; can be contralateral & ipsilateral (due to indentation of the contralateral cerebral peduncle by the edge of the tentorium cerebelli).

Eye movement; prognostic guide.

Neuro-Surgery

Basal skull fracture signs:Anterior fossa fracture:

◦CSF rhinorrhoea (nasal CSF discharge).◦Bilateral periorbital hematoma.◦Subconjuncival hemorrhage.

Petrious fracture:◦Bleeding from external meatus.◦CSF otorrhoea (CSF from external meatus).◦Battle’s sign; bruising over the mastoid.

Neuro-Surgery

Epidural hematoma:It often occurs due to a fractured temporal or parietal

bones lacerating the middle meningeal artery & vein. It can be also due to any tear in dural venous sinus.

Signs and symptoms; due raised ICP causing deteriorating consciousness level, hypertension+bradycardia, focal neurological signs (e.g. hemiparesis).

Diagnosis; lens shaped collection on CT, lumbar puncture is contraindicated.

Management; ‘horse shoe’ craniotomy flap, burr hole, ligation of the bleeding vessel, measures to lower ICP.

Neuro-Surgery

Epidural hematoma on CT

Neuro-Surgery

Epidural hematoma on MRI

Neuro-Surgery

Subdural hematoma:There may be history of trauma or not because it

may be forgotten because it was so minor or so long ago.

The elderly are most susceptible, as brain atrophy makes bridging veins vulnerable.

Signs & symptoms; headache, personality change, physical & intellectual slowing, seizures, neurological symptoms, etc…

Diagnosis; finding crescent-shaped collection over hemisphere on CT.

Management; irrigation/evacuation, via burr twist drill and burr hole craniostomy.

Neuro-Surgery

Subdural hematoma on CT

Neuro-Surgery

Subdural hematoma on MRI

Neuro-Surgery

Raised Intracranial pressure:MONRO KELLIE DOCTRINE (An increase in

one constituent or expanding mass within the skull results in an increase in intracranial pressure).

Causes:◦Expanding mass. ◦Increase in brain water content.◦Increase in cerebral blood volume.◦Increase in CSF.

Neuro-Surgery

Features:◦Headache.◦Vomiting.◦Papilloedema.

Complications; brain shifts:◦ Tentorial herniation.◦ Subfalcine herniation.◦ Tonsilar herniation.

Investigations; CT, MRI, etc...

Neuro-Surgery

Treatment:RestPositionSedationSteroidsHyper-osmotic solutionsHyperventilationSurgery, CSF drainage.

Neuro-Surgery

Hydrocephalus:Classification:

◦Obstructive; CSF flow obstruction within the ventricular system.

◦Communicating; CSF flow obstruction out/with ventricular system (with subarachnoid communication).

Signs & symptoms; mainly due to raised ICP.Investigations; CT, ultrasound, skull X-ray,

isotope cisternography, etc…Management; drainage, shunts.

applied neurosciences

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