Nincs diacm

1
Consciousness Defined by philosophy, psychology,
psychiatry and neurology. Awareness, alertness,
wakefulness Consciousness awekening from sleep
caused by recognizing and using our external
stimuli memory (eyes opening, changing
behaviour) Structural basis ARAS,
thalamocortical thalamus, limbic system,
connections cortex
2
(No Transcript)
3
Lesion of the paramedian region Various clinical
signs due to reciprocal connections with
cortical (prefrontal, limbic, paralimbic) and
subcortical (brainstem, hypothal., basal ggl,
basal forebrain, tectum, spinal cord)
structures. VMP motor thalamus motor
signs MD ARAS disturbed consciousness Reticul
ar nucleus ARAS disturbed consciousness Intrala
m. synch.-desynch. sleep disturbance Nucleus cort
ical activity cerebellum LGN gaze
disturbance Cajal nu. oculomot.nucl. ptosis,
mydriasis Anter.nucl. thalamo-frontal thalamus
dementia, memory dist., thalamo-limbic emotiona
l lability, irritability, agression,apathy,
disturbed abstract thinking
4
Types of disturbed consciousness Hypnoid Somnol
ence, Sopor, Coma Non-hypnoid Delirium Perman
ent vegetative state (appallic sy.) Akinetic
mutism Locked-in syndrome IS NOT
UNCONSCIOUSNESS!!!!!!!
5
(No Transcript)
6
The prognosis of coma Coma caused by structural
lesion death in 70 of the patients within 1
yr. Sopor 37 Somnolence 34 Severe
structural lesion without coma death in
18 of the patients Complete recovery is
possible after coma caused by alcohol and drug
intixication, hypoglycaemia, uremic or hepatic
coma, epilepsy, SAH
7
The main causes of unconsciousness Structural B
rainstem Hemispheres Diffuze multifocal (mixed
symptomes, but pupillary reflexes are usually
intact vasculitis, embolisation prion,
encephalitis, meningitis, SAH) Functional or
metabolic Anoxia, Ischemia, Endocrine
(myxoedema, hypophysis) Hepatic, Uremic
etc. Comameningeal irritation Meningitis or
SAH Comafocal signsmeningeal irritation?
abscess, contusion, meningo-encephalitis
8
Eye movement abnormalities in coma 1. Upward
gaze diminished (eyes turned downward) lesion at
the border of diencephalon and mesencephalon 2.
Conjugated movements are present the FLM is
intact 3. Skew deviation On the side of upward
turned eye the FLM is damaged.Onthe side of
downward turned eye the brachium pontis or the
dorsolateral part of medulla oblongata is
affected. 4. In apallic state The eyes follow
the moving objects, but there are no eye
movements on command. 5. Ocular bobbing the
damage is in the caudal part of the pons 6.
Roving eye movements Both hemispheres are
involved.
9
VESTIBULAR FUNCTIONS 1. Dolls eye phenomena if
the brainstem is intact turning the head causes
turning of the eyes in the opposite direction. In
the case of brainstem damage the eyes do not turn
(they are fixed like the eyes of a doll). 2. Cold
water caloric reaction it is normal, if both
eyes move toward the stimulated side. If the FLM
is damaged only the ipsilateral eye moves. If
there is no eyemovement the lesion is in the
corpus restiforme. MOTOR FUNCTIONS 1.
Coordinated movements 2. Mass movements 3. Muscle
tone changes decorticate posture
(diencephalon) decerebrate posture
(mesencephalon)
10
(No Transcript)
11
Pathological respiration types in
coma Cheyne-Stokes regularly changing periods
of Diencephalon hyperpnoe and apnoe
Central neurogenic Constant, fast, deep
hyperpnoe Upper pontine hyperventillation
tegmentum Apneusic Long inspiration
followed by a Lower part of 2-3 s delay
before expiration the pons Atactic (Biot
type) Absolutely irregular Medulla
12
Glascow Coma Scale Total Score E M V
(Score of 3-15 possible) Points Eye
opening (E) Spontaneous 4 To speech
3 To pain 2 Nil 1 Motor
response (M) Obeys 6 Localizes
5 Withdraws (flexion) 4 Flexion
posturing 3 Extension posturing
2 Nil 1 Verbalization (V) Oriented
5 Confused conversation 4 Inappropriate
words 3 Incomprehensible sounds
2 Nil 1
13
Historical Features Suggesting Structural vs.
Metabolic Coma Suggests Structural Suggests
Metabolic Sudden observed onset History of
major medical Preceding hard neurologic illness
symptoms Liver Diplopia Renal Vomiting
Pulmonary Vertigo Previous history of
overdose or Bleeding diathesis severe
depression Chronic alcoholism Known drug
abuse Previous brain lesion Stroke Tumor Subdur
al
14
Clues from the General Examination Suggesting a
Structural Lesion of the Nervous
System Clue Diagnosis Suggested Hypertension
Increased intracranial pressure (ICP) or
cerebellar mass Bradycardia Same Other
arrhythmias without cardiac arrest Same Fever
Brain abscess Purulent infection of the face or
sinuses Brain abscess Trauma Subdural hematoma
(SDH)Bleeding Intracranial hemorrhage or
SDH Tumor Metastasis
15
HERNIATIONS I. CENTRAL usually caused by
diffuse brain oedema apathia, somnolence hicups
Cheyne-Stokes respiration pupils are normal in
seize, reactive to light roving eye
movements no dolls eye phenomena pain evokes
mass motor reaction
16
HERNIATIONS II. UNCAL (TRANSTENTORIAL) space
occupying lesion in one hemisphere displacement
of brain structures across the midline through
the opening of the falx the ipsilateral uncus
gyri hippocampi presses the oculomotor nerve
against the sphenopetrosal fold, causing
ipsilateral dilatation, ptosis pyramidal signs
and paresis on the contralateral side, later on
both sides apathia nausea vomiting brainstem
damage causes decerebration and central
herniation
17
HERNIATIONS III. FORAMINAL caused by posterior
fossa space occupying lesion the cerebellar
tonsils are pressed in to the foramen magnum
causing the compression of the lower brainstem e
arly sign is abnormal respiration decerebration
18
(No Transcript)
19
Apallic syndrome Severe cortical lesions in both
hemispheres (anoxia, hypoglycaemia, liver
malfunction, uraemia, traumatic contusion). The
patien seems to be awake, but he is not aware of
himself or the environment. The eyes do not
follow moving objects. Normal sleep-wake
cycle. All vegetative functions are
preserved. Decorticate rigidity Liberation
signs Pyramidal signs on both sides Increased
vegetative reactions (salivation, high heart
rate, tachypnoe, sweting).
20
Akinetic mutism Lesions in the midline of pons,
bilateral frontal lobe damage, thalamus
damage. The patient does not move. The eyes are
open and do follow moving objects (preserved
cpnjugated eye movements.) Normal sleep/wake
cycle.
21
LOCKED IN SYNDROME It is not unconscious state,
but due to differential diagnostic problems it
has to be discussed. Damage in the pons basis,
most frequently caused by basilar occlusion.
(the tegmentum is intact) Tetraplegia. Vertical
eye movements preserved. Blinking can be carried
out (this way yes/no questions can be answered).
22
DELIRIUM The awereness is preserved, but the
content is disturbed. Behavioural changes,
desorientation Visual, acoustic and haptic
hallucinations Disturbed intellectual
functions Disturbed memory functions
23
Questions to be answered when examining
unconscious patient 1. Is the autonomic
regulation intact? 2. Is it hypnoid or
non-hypnoid condition? 3. Are there focal
neurological signs present? hemispheric
origin? brainstem origin? 4. Are there
simmetrical signs present? cortical
decortication posture, liberation signs,
anxiety brainstem decerebration, gaze
disturbance, pathological pupillary reflexes
24
Diagnostic procedures 1. EEG a) metabolic
disturbance b) epilepsy c) drug 2. Imaging (CT,
MR) structural changes, subarachnoid hrg., sinus
thrombosis 3. Lumbal puncture meningitis,
encephalitis 4. Ultrasound of extra- and
intracranial vessels occlusion- might be treated
with thrombolysis 5. Laboratory tests metabolic
disturbances
25
Encephalopaties I. Etiology Neurologic
signs Diagnosis Hypoxia decortication
posture, cardiac causes, pyramidal
signs,excitation polytraumatisation suicide
Hyperosmolar epileptic attack., focal
signs plasma sugar level diab. coma above
16mmol/l high serum osmolarity Diabetic
ketoacidosis obtundation ketonuria, plasma
sugar level above 30 mmol/l Hypoglycaemia
vegetative state or coma, se. sugar below 1.5
epileptic seizures, focal signs Hepatic tre
mor, asterixis, obtundation, se. ammonium
high delirium, vegetative state Uraemia ep
ileptic seizures, myoclonus creatinin, K, Na,
CN eventually coma
26
Encephalopaties II. Hyponatraemia obtundation,
GM seizures, se Na below 126 after too fast
correction central pontine myelinolysis Hypern
atraemia delirium, muscle weakness, se Na above
156 disturbed consciousnes Hypercalcaemia del
irium, muscle weakness se Ca and
parathormone high Hypocalcaemia tetany,
delirium, GM seizures se Ca and
parathormone low Lack of thyamine
obtundation, ocular signs, Wernicke
enceph. hypnoid unconsciousnes
27
Hypoglycaemic coma Causes starwing, alcohol,
insulin Signs Obtundation, disorientation,
liberation signs, decortication posture,
myoclonus, epileptic seizure. Vegetative state
and coma might be present at the same
time. Differential diagnosis in hypoglycaemic
coma the pupillary reaction are intact, while in
brainstem lesion they are lacking.
28
(No Transcript)
29
(No Transcript)
30
(No Transcript)