neurological symptomatology part ii
DESCRIPTION
Neurology Lecture: Symptoms of neurological diseases part IITRANSCRIPT
Altered Consciousnss
Consciousness
awareness of the environment and oneself an awake and alert condition one is capable of perceiving whats happening in the surroundings ability to respond in an appropriate manner to certain stimuli
components of consciousness: 1. arousal and wakefulness - functions of the ARAS and its projections 2. awareness or the content of consciousness - function of the cerebral cortex representing cognitive mental functions
Structures comprising the Consciousness System:1. Reticular formation 2. Neurochemically-defined nuclear groups of the brainstem 3. Thalamus and the thalamic nuclei 4. Thalamocortical pathway (tract) 5. Basal forebrain 6. Cerebral cortical areas
Levels of Depressed Consciousness:E. Benarroch, B. Westmoreland, et al: Medical Neurosciences, 3rd ed.
1. 3.
Alert Confused - transient decline in cognitive functions in the presence of normal arousal; decreased level of attention; impairment of clear thinking - patient is easily arousable; appropriate verbal and motors responses to sensory stimuli; when left alone patients drifts to sleep state - alertness is mildly or moderately decreased; when left alone, patient drifts back to sleep state; when aroused, shows slow response to any stimuli - moderate amount of spontaneous movements, and can be aroused to respond purposefully to afferent stimuli; can give brief responses to questions or simple commands - state of extended unconsciousness; unarousable, little or no response to pain or noxious stimuli
7.
Somnolent
4.
Obtunded
15. Stupor
6.
Coma
Levels of Depressed Consciousness:M. Victor, A. Ropper: Adams and Victors Principles of Neurology, 7th ed.
1. 3.
Alert Confused - clouding of consciousness; some degree of inattentiveness and disorientation mildly confused moderately confused severely confused - inability to sustain a wakeful state without the application of external stimuli; indistinguishable from light sleep - can be roused only by vigorous and repeated stimuli, at which time, patient opens his eyes, looks at the examiner, and does not appear to be unconscious - incapable of being aroused by external stimuli semi-coma deep coma
9.
Drowsiness
12. Stupor
5.
Coma
Levels of Depressed Consciousness:B. Bates: Techniques of Physical Examination, 3rd ed.
2. 2.
Alert Confused - mild diminution of consciousness with mental slowness, inattentiveness, dulled perception, incoherent thought process, patient is disoriented - marked reduction in mental and physical activity, marked slowness and reduction in response to commands or stimuli - complete loss of consciousness with unresponsiveness to stimuli and voluntary movements
3. 4.
Stupor Coma
Levels of Depressed Consciousness:W. Demyer: Techniques of the Neurological Examination, 3rd ed.
1. 3. 6.
Alert Somnolence Semicoma - patient can be aroused to a normal level of awareness - patient can be aroused to some degree, but cannot reach or sustain a normal level of consciousness lethargy stupor - patient cannot be aroused partial coma deep coma
13. Coma
Glasgow Coma ScaleEye Opening Never To pain To verbal stimuli Spontaneous Best Verbal response No response Incomprehensible sounds Inappropriate words 3 Disoriented Oriented and converses Best Motor Response No response Extension/Decerebrate Flexion/Decorticate 3 Flexion withdrawal Localizes Pain Obeys command
1 2 3 4 1 2 4 5 1 2 4 5 6
Clinical Approach to a Comatose Patient
1.
Airway-Breathing-Circulation Endotracheal intubation / oropharyngeal tube Intravenous fluids Do: a rapid neurological assessment while addressing the vital functions Do: initial ocular survey of the organ-systems of the body while addressing A-B-C
2. General Physical Examination signs of head injury look for meningeal signs of irritation
Clinical Approach to a Comatose Patient
1.
Neurological Assessment Always Inspect! Note for limb movement asymmetry position of head and eyes; facial grimacing to a given stimulus state of responsiveness / level of consciousness / GCS involuntary movements of limbs abnormal posturing
Decorticate Posturing Vs Decebrate posturing
Clinical Approach to a Comatose Patient
4.
Neurological Assessment Inspect! abnormal breathing patterns
Sites of the lesions: 1. 2. 3. 4. Cheyne-Stokes respiration - cerebral hemisphere CNH - midbrain Apneustic Breathing - upper pontine level Ataxic Breathing - medulla oblongata
Clinical Approach to a Comatose Patient
5.
Neurological Assessment
- check pupil responsespin point - pontine hemorrhage; opiate poisoning bilaterally fixed mid position - midbrain lesion unilateral or bilateral fixed and dilated - supratentorial mass with uncal herniation enlarged, slowly reactive pupils - metabolic causes
- examine ocular movementsdo: oculocephalic reflex oculovestibular reflex
- examine the fundi (fundoscopic examination)look: papilledema; subhyaloid hemorrhage
Useful guide in the examination of the brainstem/cranial nerve functions in a comatose patient
Cranial nervesII and III III, IV, VI, and VIII Absent pupillary reflexes Absent oculocephalic reflex (Dolls eye maneuver)the eye moves passively in the direction of the horizontal or vertical eye movements, rather than maintaining their positions of gaze while the head is being moved by the examiner
V and VII VIII, III, and VI
Absent corneal reflexes No facial grimacing to deeply painful facial pain Absent water caloric reflexes (oculovestibular responses)an intact reflex consists of transient tonic deviation of the eyes towards the stimulated side when stimulated with cold water
IX and X
Absent gag reflexno cough or gag in response to pharyngeal or tracheal stimulation and suctioning
Absence of any respiratory effort, even after fully oxygenating the patient and then allowing the pCO2 to rise to 50-60 mmHg (apnea test)
Altered Consciousness
TransientLoss of consciousness
loss or episodic alteration of consciousness
Persistentcomatose state Transient loss of consciousness seizures syncope cerebral ischemia / vertebrobasilar ischemia carotid sinus disease drop attacks sleep disorders metabolic (hypoglycemia)
Differential Diagnosis of Transient Loss of ConsciousnessSeizures Syncope
can occur in any position and time of the day Preceding aura may be present Sudden-onset Urinary or fecal incontinence may be present Tongue bitting Post-ictal confusion, drowsiness, and headache
upright position usually prodrome light headed, nausea, ringing in the ears, dimming of vision, pallor, sweating hypotension and thready pulses relatively rapid recovery
Situational syncope: Emotion or pain Micturition Coughing Postural
Cardiac causes of syncope:
Left or right ventricular outflow obstruction Arrhythmias pump failure
Differential Diagnosis of Transient Loss of ConsciousnessClinical Features Vertebrobasilar ischemiaAdditional brainstem symptoms (eg vertigo, diplopia) Cerebrovascular risk factors Peripheral pulses involvement Syncope on turning head or neck or on neck massage Postural hypotension confirmed on tilt table testing Elderly females No alteration of consciousness state Rapid recovery Episodic Normal examination and investigation Anxiety or situational (eg. Crowded rooms) Perioral and/or digital tingling sensation, carpopedal spasm, chest pain High respiratory rate, low pCO2, metabolic alkalosis Inappropriate desire to fall asleep Falls with emotional situations, eg. Laughing Family history Diabetic on treatment or relative of such a patient Hepatic failure Hypopituitarism, Addisons disease Insulinemia; glycogen storage disease Excess alcohol
Carotid sinus disease Drop attacks
Hyperventilation
Sleep disorders narcolepsy cataplexy Metabolic (hypoglycemia)
Intracranial Causes of Persistent Alteration of ConsciousnessIntracranial Causes Epilepsy Clinical FeaturesConvulsions that are clinically unequivocal May have incontinece Tongue biting and other injuries may be present Evidence of head injury or presence of basal skull fracture Remote history of head injury (several weeks or even months) Elderly patients and alcoholics are at particular risk, eg prone to accidental falls History of sudden severe/explosive headache Associated with an initial loss of consciousness (collapse) Presence of fever (central in origin) Neck rigidity; presence of meningeal irritation Focal neurological deficits particularly if with intracerebral extension or complications Presence of focal neurological deficits that are maximal at the onset May have headache, profound alteration of consciousness at the onset Presence of hypertension, retinopathy, seizures Sudden-onset diffuse (not focal) neurological deficits
Head trauma extradural or epidural hemorrhage subdural hemorrhage Cerebrovascular diseases Subarachnoid hemorrhage
Intracerebral hemorrhage Hypertensive Encephalopathy
Intracranial Causes of Persistent Alteration of ConsciousnessIntracranial Causes Clinical Features
Infection of the CNS Meningitis Encephalitis
Headache prominent early in the course; fever; signs of meningeal irritation Seizures (early encephalitic signs are prominent); fever; presence of profound signs of altered consciousness Subacute-onset; headache may be present Focal neurological deficits are present Obvious signs of infections in the contiguous structures
Cerebral abscess
Extracranial Causes of Persistent Alteration of ConsciousnessExtracranial Causes Circulatory collapse Cardiac causes (arrhythmia, myocardial infarction) Septicemic shock Hypovolemia (blood loss) Metabolic causes Hypo-or hypernatremia Hypo- or hyperkalemia Hypo- or hyperglycemia Some Prominent Clinical FeaturesHypotension, tachycardia, rhythm disturbances; cardiac failure May be preceded by cardiac manifestations (eg. Chest pain; dyspnea) Rigor, pyrexia, vomiting, peripheral vasodilation Obvious source of infection from some other organ system Obvious clinical source of blood loss; tachycardia, pale appearance Muscle twitches, dehydration Cardiac muscle excitability, ileus, diabetes insipidus
Hemiplegia (reversible), seizures Dehydration, hyperventilation, ketotic breath Bradycardia/ initially tachycardia, hypotension, hypoventilation, rigidity, cardiac arrest Sallow skin, pale mucosae, hypertension
Hypo- or hyperthermia Uremia
Extracranial Causes of Persistent Alteration of ConsciousnessExtracranial Causes Metabolic Causes Hepatic failure Hypoxia HypercapniaJaundice, signs of portal hypertension, GI bleeding, sepsis
Some Prominent Clinical Features
Following respiratory failure, cardiorespiratory arrest, irreversible brain damage will occur after 4 minutes of anoxia Pink puffer, bounding pulses, papilledema, asterixis
Endocrine Adrenal Crisis Hypopituitarism
Hypotension, abdominal pain, buccal and flexor pigmentation Pallor, hypogonadism, bitemporal hemianopsia
Extracranial Causes of Persistent Alteration of ConsciousnessExtracranial Causes Circulatory collapse Cardiac causes (arrhythmia, myocardial infarction) Septicemic shock Hypovolemia (blood loss) Metabolic causes Hypo-or hypernatremia Hypo- or hyperkalemia Hypo- or hyperglycemia Some Prominent Clinical FeaturesHypotension, tachycardia, rhythm disturbances; cardiac failure May be preceded by cardiac manifestations (eg. Chest pain; dyspnea) Rigor, pyrexia, vomiting, peripheral vasodilation Obvious source of infection from some other organ system Obvious clinical source of blood loss; tachycardia, pale appearance Muscle twitches, dehydration Cardiac muscle excitability, ileus, diabetes insipidus
Hemiplegia (reversible), seizures Dehydration, hyperventilation, ketotic breath Bradycardia/ initially tachycardia, hypotension, hypoventilation, rigidity, cardiac arrest Sallow skin, pale mucosae, hypertension
Hypo- or hyperthermia Uremia
In all comatose patient, attempt to rule out the following conditions: 1. Locked-in syndromelesion in the ventral pons affects: corticobulbar and corticospinal tracts patient is awake but unable to respond patient communicates via vertical eye movements and blinking
2. Persistent vegetative stateusually secondary to severe cerebral injury patient recovers partially from a comatose state no purposeful movements and no demonstrable cognitive functions
In all comatose patient, attempt to rule out the following conditions: 3. Catatoniasilent, no volitional movements no emotional response to external stimuli patient resists an examiners attempt to move; patient maintains limbs in fixed position seen in schizophrenic catatonic state
4. Non-convulsive status epilepticussuspect this condition in patients who dont regain consciousness after a convulsive status epilepticus
End of segment
SEIZURE
Seizuresresult from abnormal, sudden, excessive and asynchronous electrical discharges from the cortical neurons the discharges are self-terminating and have a tendency to recur
Ictus Aura
- the seizure event itself - the subjective sensation or any phenomenon that precedes and marks the onset of the epileptic seizure Prodrome - refers to premonitory changes in mood or behaviour, may precede the attack by some time Epilepsy - recurrent seizure events with defin ite etiological factor/s Convulsion - seizure events with motor manifestations
Seizures
Seizures
Partial seizures- deviation of the head and eyes to one side (aversive seizure) points to an irritative focus in the opposite prefrontal region
- in simple partial seizures, consciousness is often preserved (see video) - Jacksonian seizure starts as a clonic movement in one portion of the body, usually the thumb, corner of the mouth, or great toe, and spreads to adjacent muscular groups over a few seconds or minutes - the seizure event may persist on one part of the body or may become generalized
Complex partial seizures -differs from generalized motor seizures by:1. frequent occurrence of an aura that arises from discharges in the autonomic, visceral, olfactory portions of the temporal lobe and limbic system 2. loss of awareness or contact with the environment, often associated with behavioral or complex motor movements for which the patient is amnesic after the attacks
Complex partial seizures
Complex partial seizures
- subjective experiences of the aura:hallucinations (olfactory, gustatory, visual, auditory) illusions (space distortions, shrinkage, or angulations) aberrations in cognition (dj vu, sense of familiarity) affective changes (anxiety, fear, rage)
- the seizure may terminate with only the subjective component or may progress to the motor phase evident by repetitive motor acts (chewing, lip smacking, undressing, incoherence)
Tonic-clonic (grand mal) seizures- abrupt-onset, w/o warning; usually begin with opening of the eyes and mouth, flexion and abduction of the arms, and extension of the legs tonic phaseheralded by contraction of the respiratory muscles resulting in vocalization; followed by closure of the jaw, respiratory arrest with cyanosis, and sphincter incontinence persists for about 15-30 sec. followed immediately by the clonic phase
clonic phaseviolent, rhythmic muscular contractions affecting the whole body and respiratory muscles eye movements, facial grimacing, persistent apnea lasts for about 1-2 min.
Tonic-clonic (grand mal) seizures
Absence seizures- brief; loss of contact with the environment accompanied by minimal motor manifestations - abrupt in onset and described as a stare or cessation of an ongoing behavior - may be accompanied by fluttering of the eyelids or by few facial twitches - full recovery is evident after 5-10 sec.
Absence seizures
Etiology epilepsy is a symptom and sign of numerous neurologicaldisorders over 50% of patients have no apparent cause can be found despite full and extensive investigation etiology will greatly vary depending on: - the age of the patient - surrounding circumstances in the history
Causes of seizures
The following are the most common differential diagnoses In a patient presenting with seizures: syncopal attackscardiac arrhythmias, carotid sinus hypersensitivity, vasovagal attacks, postural hypotension present are: prodromal pallor, nausea, vomiting, sweating, palpitations
pseudoseizures
hysterical, attention-seeking, feigned seizures are common especially in patients with known seizures vital signs, pupils, pO2 and serum pH remain unchanged, plantar responses are normal, the EEG will reveal normal findings and no postictal cortical activity slowing
transient ischemic attacks / cerebrovascular diseases metabolic causes, eg. hypoglycemia
End of segment
Dementia Dementia (WHO ICD-10) a disorder characterized by both memory and thinking deterioration sufficient to impair personal activities of daily living; the memory impairment affects the registration, storage and retrieval of new information
not a disease entity, rather a symptomatology with varied etiology and clinical presentation impaired consciousness implies delirium rather than dementia the most common causes are Alzheimer and Vascular dementia, both are seen in advanced age groups
Common types of dementing diseases and their approximate frequenciesDementing Diseases Cerebra atrophy, mainly Alzheimer but including Lewybody, Parkinson, Pick Multi-infarct dementia (Vascular type) Alcoholic dementia Intracranial tumors Normal-pressure hydrocephalus Huntington chorea Chronic drug intoxications Miscellaneous (hepatic failure, pernicious anemia, thyroid diseases,ALS, Creutzfeldt_jacob disease, MS)
% 50 10 7 5 5 2 3 6 2 2 8
Head trauma AIDS dementia Pseudodementias (depression, hypomania, schizophrenia,hysteria, undiagnosed)
M. Victor and A Ropper: Adams and Victors principles of Neurology 7th ed.
Dementia
General clinical features: The earliest feature of dementia, from most causes, is loss of memory for recent events. Subsequent symptoms include abnormal behavior, loss of intellect, mood changes, and difficulty coping with ordinary routines. Rate of progression: Alzheimer disease Vascular dementia Encephalitis - slowly progressive over years - progressive but often fluctuating or stepwise with each stroke - over days to weeks
Some reversible forms of dementia: Endocrinologic Metabolic Hydrocephalic Tumors Hypothyroidism Hypoparathyroidism Hepatic Encephalopathy Vit. B12 deficiency Post-infectious NPH Meningiomas
Pseudodementia Major Depression
Things to emphasize in the History and Examination of a demented patient:It is essential to get a history from a relative or friend, as well as from the patient in order to gauge the following rate of intellectual decline activities of daily living and social interaction nutritional status drug history general health and relevant disorders, eg. Stroke, head injury family history of dementia
Neurologic evaluation should focus more on the following presence of focal neurologic deficits involuntary movements pseudobulbar signs presence of primitive reflexes, eg. Pout, grasp reflexes gait disorder
Things to emphasize in the History and Examination of a demented patient:Neurologic evaluation should focus more on the following presence of focal neurologic deficits involuntary movements pseudobulbar signs presence of primitive reflexes, eg. Pout, grasp reflexes gait disorder
In all patients suspected with dementia, it is essential to utilize the Mini-mental State Scale
Probable dementia = 24-27 score
Primary degenerative dementia: 1. Alzheimer disease 2. Pick disease 3. Lewy-body dementia
Alzheimer disease accounts for more than of patients with dementia at least of the population over 85 years have Alzheimer Clinical symptomatology: short term memory loss > long term memory personality changes depression anxiety other psychological features
Alzheimer disease Clinical signs:Early stages - will reveal very little clues - slight confusion on dates and location of the interview - speech can be a little hesitant - no focal neurological deficits Later stages - as the disease progresses, problems in language, praxis and gnosis become increasingly apparent - personal care deteriorates - primitive reflexes emerge - eventually, the patient becomes mute, bed-bound and incontinent - condition generally lasts 7-15 years
Parting words on Alzheimer disease typically, a patient with Alzheimer disease does not initiate the consultation there are seldom any focal neurological signs at the time of the first assessment formal psychometry is usually essential to confirm the diagnosis, rather than relying only on the screening test such as the MMSE scale the main role of brain imaging in the assessment of Alzheimer Is to exclude other treatable or revesible dementias
End of segment