Dizziness & Vertigo

The most frequent complaints among OPD Dizziness-imbalance,headache,back pain, fatique,Mostly benign,Analyse correctly the nature of disturbance and anatomic location,A feeling of rotation,whirling,non-rotatory swaying,weakness,faintness,unsteadiness,Dizziness may mean giddiness,light head- edness,unsteadiness,swimminess,vertigo.

The specific qualities of vertigo : all subject ive and objective illusion of motion/position

Pseudo vertigo : non-rotatory giddiness

n  Bipolar

¨  Peripheral terminate in hair cells crista ampu llaris SCC & macula acusticae Saccule-Utricle

¨  Central via internal auditory meatus+cochlear + 7^th, terminate in the vestibular nuclei (sup-Bechterew, lat-Deiters, med-Schwalbe, inf).  Some fibre from SCC project directly to the flocculonodular lobe+ adjacent vermian cortex cerebellum via the juxtarestiform body 

SCC horizontal is inclined upwards 30° from the horizontal plane, detect turning

The utricle is a gravity-operated receptor which responds to tilting (out of position R)

The saccule responds to acceleration

The utricle-saccule system provides inform ation leading to correct vertical postures when sits,stands and walks

¨  Efferent fiber from cerebellum to i.l. vestibular and fastigial nucleus

¨  Efferent fiber from fastigial ncl to c.l. vestibular nuclei via juxtarestiform body

¨  Lateral and medial nuclei have important connection with the spinal cord via the uncrossed lateral vestibulospinal tract (limb muscles) and via the crossed and uncrossed medial vestibulospinal tract (axial muscles)

¨  Superior and medial nuclei influence 3^rd 4^th 6^th CN 

¨  All vestibular nuclei have afferent and efferent connections with pontin RF à subserve Vestibulo Ocular (clear vision) and Vestibulo Spinal reflex (stable posture)

¨  There are projection from the vestibular nuclei to Cerebral Cortex (intra parietal sulcus and superior Sylvian gyrus)

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INFARCTION STROKE

INFARCTION STROKE

MECHANISM OF ISCHEMIC INFARCTION

1. Thrombotic

Ø  Thrombotic infarction occurs when a thrombus superimposed on an atherosclerotic plaque

Ø  May be precipitated by an abnormality of blood cloting

2. Embolic

Ø  Occlusion of an arteri by an embolus

3. Hemodynamic

Ø  Severe stenosis or occlusion of the proximal arteries

Ø  Collateral compensatory blood flow is inadequate

Ø  Global cerebral perfusion is critically decreased          ( e.g. cardiac output decreased )

CLINICAL CATEGORIES

1. Atherothrombotic infarction

Ø  Medical history è one or more risk factors

Ø  Headache and vomiting are unusual

Ø  The onset come rapily, may continue to worse over hours or days

Ø  The trombus is superimposed on the atherosclerotic plaque

Ø  Atherosclerotic plaque è extracranial or intracranial arteries

Ø  There are 2 mechanisms :

a.       Atherosclerotic plaque enlarge è stenotic / occlusion

b.      Embolism or plaque fragments è occlusion ( artery – to – artery embolus )

CLINICAL CATEGORIES

2. Cardioembolic

Ø  The onset is rapid, focal deficit completely and may worsening

Ø  Usually at activity

Ø  The source of embolus :

ü  Cardiac conditions :

v  Atrial fibrillation, acute myocardial infarction, congestive heart failure, mitral or aortic valve disease

ü  Transcardiac conditions ( paradoxical embolus )

v  Right to left cardiac shunt

v  The source of clot : peripheral venous thrombus

Ø  Sometimes clinical finding; isolated homonymous hemianopsia or isolated aphasia

Ø  Brain imaging :

ü  Involve the cortex, commonly in the distribution of branches of the MCA

ü  Possible haemmorhage infarction

3. Lacunar infarction

Ø  Small lesions, involvement of deep, small, penetrating arteries

Ø  The arteries to branch at 90⁰ ( e.g. lenticulostriate arteries and brain stem )

Ø  The causes are :

ü  Poor collateral connection

ü  Blood obstruction by arterial disease

ü  Thrombus

ü  Embolus

READ MORE - INFARCTION STROKE

STROKE -Clinical Manifestasion

CEREBROVASCULAR DISEASE :

1. Asymptomatic
2. Focal brain dysfunction

Ø  TIA ( Transient ischemic attack )

Ø  Stroke

3. Vascular dementia
4. Hypertensive encephalopathy

STROKE

Ø  Definition :

                Stroke is brain dysfunction, sadden and very rapid development of symptoms, focal or global, caused by only primary cerebrovascular disease which persistence of the neurologic deficit for longer than 24 hours or die.

Ø  Primary cerebrovascular disease is refere to the risk factors

Ø  Global brain dysfunction is refere to unconsciousness status

Ø  TIA if neurologic deficits last completelly less 24 hours

Improving stroke

Ø  Complete recovery of neurologic deficit between 24 hours to 3 weeks

Worseningstroke

Ø  Progresivity of nneurologic deficit, qualitative and quantitative, either anamnestic or follow up

Ø  50 % of cases in several minutes and hours

Ø  Divided in :

ü  Smooth worsening

ü  Steplike worsening

ü  Fluctuating worsening

CLINICAL MANIFESTATION ( cont’ )

1. Carotid system

Ø  Visual disturbances

ü  Contralateral homonymous hemiamianopsia

ü  Amaurosis fugax ( TIA )

Ø  Higher cortical dysfunction

ü  Aphasia

ü  Agnosia

CLINICAL MANIFESTATION ( cont’ )

2. Vertebrobasiler system

Ø  Visual disturbances

ü  Homonymous hemianopsia

ü  Cortical blindness ( TIA : blackout )

Ø  Others

ü  Loss of balance

ü  Vertigo

ü  Diplopia

READ MORE - STROKE -Clinical Manifestasion

EPILEPSY

Definition

Abnormal and recurrent excessive synchronized discharge of cerebral neuron with clinical manifestation of epileptic seizure which are an intermittent stereotypical behavior, emotion, motor function or sensation.

Pathophysiology

•       Paroxysmal depolarization shift (PDS) of the resting membrane potential, which triggers a brief rapid   burst of action potentials terminated by a sustained after hyperpolarization

•   PDS : result of imbalance between excitatory (glutamate and aspartate) and inhibitory (GABA) neurotransmitters

•         Abnormalities of voltage controlled membrane ion channels

•        Imbalance between endogenous neuromodulators, acetylcholine favoring depolarization and dopamine enhancing neuronal membrane stability

Focal Epiloptogenesis

•          Asynchronous burst firing in some hypocampal and cortical neurons

Generalized Epiloptogenesis

·         asynchronous burst firing in abnormal thalamocortical interaction

Etiology

•          Idiopathic

•          Cryptogenic

•          Symptomatic

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Cerebral Disorders

Normal cerebellar function

Responsible for muscle synergy (coordination) throughout the body

Coordinates the action od muscles and times their contraction à movement smoothly and accurately

As a monitor of other center of the brain (not the iniator!)

The modulator (regulator) of motor activities; integrated with :

•          Vestibular system (maintain muscle tone and equilibrium)

•          General proprioceptive and exteroceptive receptors

•          Auditory and visual system

Basically a somatic afferent organ !!

•          Neocerebellum

–        Dysmetria –inability to stop the movement at the desired point (overshoots or stops before it is reached)

–        Intention tremor – evident during purposeful movement, but absent/diminished with rest. Titubation : rhytmic tremor iof the head, 3-4x/minute- lesion in the midline of cerebellum

–        Postural disturbance

–        A/dysdiadochokinesis - inability to stop a movement and follow it immediately by directly opposite action

–        Hypotonia – ipsilateral to the lesion site; loss of cerebellar facilitation to the stretch reflex

–        Eye disturbance : skew deviation and nystagmus (also occurred in vestibular lesion and its connections)

–        Disturbance of articulation and phonation : scanning speech/stacatto

–        Gait disturbance : cerebellar ataxia (tend to fall to the lesion site)

•          Paleocerebellum

–        Symptoms and signs of postural and muscle tone disrturbance

•          Archicerebellum

–        Truncal ataxia (swaying while sitting)

–        Vertigo

•          Equilibratory coordination - maintanance of balance and the coordination of the body as a whole; examination of station and gait

–        Truncal ataxia, titubation

–        Romberg sign, Walk tandem

•          Non-equilibratory coordination – ability to carry out discrete, relatively fine, intentional movement with extremities.

–        Dysmetria, Dysdiadochokinesia

–        Nose-to-finger test, finger-to-finger test, heel-to-knee-to-toe test

–        Rebound test, test pointing and past pointing

–        Functional test : button-unbuttoning, writing, picking coin at desk

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COORDINATION

Cerebellum as center of coordination

- Anatomy

- Physiology

- Its disorder

Anatomy

•          Occupies most of the posterior cranial fossa

•          Dorsal to the brainstem and attached  to it by cerebellar peduncles :

–        Superior cerebellar peduncle (Brachium conjunctivum) « midbrain

–        Middle cerebellar peduncle (Brachium pontis) « pons

–        Inferior cerebellar peduncle (restiform body) « medulla oblongata

•          Other relationship :

–        The fourth ventricle

–        Tentorium cerebelli

•          Composition

–        Cerebellar hemispheres

–        Vermis : cortex and medulla (incl. Nuclei)

•          Lobes

–        Anterior lobe (palaocerebellum)

•          C/o most of the vermis and anterior aspect of hemispheres

•          Associated with proprioceptive (spinecerebellar) and exteroceptive input

•          Significant role in regulation of muscle tone (maintain posture)

–        Posterior lobe (neocerebellum)

•          The largest part; c/o main bulk of hemisphere and part of vermis

•          Receive connections of cerebrum through nuclei & brachium pontis

•          Role in muscular coordiantion of phasic movement

–        Flocculonodular lobe (archicerebellum)

•          C/o paired flocculi of hemispheres and unpaired nodulus

•          Cerebellar portion of vestibular system (somatic afferent collumn)

•          Significant role in muscle tone, equilibrium, and posture (trunk muscles)

Cerebellar cortex

•          Layers

–        Molecular layer :

•          Outer layer – synaptic integrative layer

•          Input from granular layer and deep cerebellar nuclei

•          C/o nerve fibers and some basket cell

–        Purkinje cell layer

•          Middle cell layer –Output layer to the intrinsic cerebellar nuclei

–        Granular layer

•          Innermost layer – receive input from outside

•          Cell and Nerve types

READ MORE - COORDINATION

TEST OF AUTONOMIC FUNCTION

Sudomotor function

• Starch test
• Quinarizin, a color indicator
• Quantitative sudomotor axon reflex test ( QSART test )

Hyperhidrosis

• CRPS ( Complex Regional Pain Syndrome )
• Spinal paraplegic
• Peripheral neuropathy
• Localized hyperhidrosis
• ( palm, feet, lower extremities )
• congenital
• sign of nervousness

Anhidrosis

Peripheral nerve disease

Sympathectomy Mental arithmetic

                ⓝ blood pressure & pulse rate increases

                defect sympathetic NS ® no response ( central/peripheral )

Alteration of the pupils

                + epinephrine sol ( 1 : 1000 )

                ⓝ no change

                sympathetic denervation ® dilatation

                + cocaine sol 4 %

                ⓝ dilatation

                sympathetic denervation ® no response

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THE AUTONOMIC NERVOUS SYSTEM ( ANS )

• The functional devision of the PNS
• Innervates smooth and cardiac muscle & the glands of the body
• Involuntary
• Function

Regulates “ the vital functions “ that maintain the internal environtment ( homeostasis )

The vital function :

Respiration, circulation, metabolism, body temperature, water metabolism, digestion, secretion

Hypothalamus

Controlling or steering the ANS

Rostral portion ® parasympathetic

Caudal ® sympathetic

Connect with the descending reticular system ( mid brain )

Cholinergic axons

• Preganglionic axons of the parasympathetic and sympathetic NS
• Post ganglionic neurons of the parasympathetic NS
• Post ganglionic axons of the sympathetic NS to the sweat glands & piloerector muscles

Adrenergic axons

• Postganglionic sympathetic axons
• Adrenal gland

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Cortical Function - Anatomy and Physiology

Three major operations of neurons of the CNS :

• Reception and Registration of sensory stimuli from outside and within
• Planning and execuition of complex motor act.
• Intermediary Processing ( thought,memory,language and etc)

Cerebral Hemisphere Right & Left connecting by Corpus Calosum

Cerebral Hemisphere are divided :

• Primary sensory cortex.
• Primary motor cortex
• Association cortex
• Limbic-Paralimbic cortex

Cortical function : Spesific location

Primary reseptive area
Secondary reseptive area
Association area

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Sign and Symtomps In Neurological Diseases

Due to Location

1.Central Nerves System :

- Hemisphere (Cerebral, Cerebellum, Brain Section)

- Medulla Spinallis (Cervical, Thoracal, Lumbosacral) 

 2. Peripheral Nerves System

- Nucleus

- Ganglion

- Nerve Root 

Due to Pathophysiology

1.Paralytic / Damage

2.Initative - Disturbance of Transmision

Cardinal Symtomps

1. Counsciousness

- General Cerebral Disorders

• High Intracranial Pressure
• Intoxication
• Metabolic Disorders

- Focal Cerebral Disorder

• Disturbances of ARAS / Brain Stem

2. Meningeal Irritation

• Infection
• Haemorrhage
• Radix Irritation

3. Motor Dysfunction

• Central ( Cerebral, Medullar )
• Upper Motor 
• Lower Motor
• Perifer

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