Presentation on theme: "Session 3: Cognitive Problems. Definitions Dementia: clinical state characterized by loss of function in multiple cognitive domains; diagnostic features."— Presentation transcript:
Session 3: Cognitive Problems
Definitions Dementia: clinical state characterized by loss of function in multiple cognitive domains; diagnostic features include : memory impairment and at least one of the following: aphasia, apraxia, agnosia, disturbances in executive functioning. Cognitive impairments must be severe enough to cause impairment in social and occupational functioning and there must be a decline from from a previously higher level of functioning. Acute confusional state: impairment of cognitive function that is not progressive, but is reversible. The impairment of consciousness varies, often being worse at night. It may be described as a transient organic brain syndrome characterized by concurrent disorders of attention, perception, thinking, memory, psychomotor behaviour and the sleep-waking cycle. Delirium: acute cognitive and behavioral change with attentional problems (analogous to above) Encephalopathy: diffuse brain dysfunction (includes acute confusional state and delirium) Amnestic syndrome: Partial or total loss of memory, usually resulting from shock, psychological disturbance, brain injury, or illness. (cf Bourne Identity) Mental retardation: a disability characterized by significant limitations both in intellectual functioning and in adaptive behavior as expressed in conceptual, social, and practical adaptive skills beginning before age 18. Schizophrenia: any of several psychotic disorders characterized by distortions of reality and disturbances of thought and language and withdrawal from social contact
Schizophrenia Two (or more) of the following, each present for a significant portion of time during a 1-month period (or less if successfully treated): –delusions –hallucinations –disorganized speech (e.g., frequent derailment or incoherence) –grossly disorganized or catatonic behavior –negative symptoms, i.e., affective flattening, alogia, or avolition. Note: Only one symptom is required if delusions are bizarre or hallucinations consist of a voice keeping up a running commentary on the person's behavior or thoughts, or two or more voices conversing with each other.
Man found down BP: 116/68; 104 HR; 99.5 F; 14 RR Opens eyes to voice; grimaces to pain; unable to follow commands; blinks to threat bilaterally Normal oculocephalics; symm reactive pupils; facial symmetry Reduced tone with withdrawal of all extremities to pain
Laboratory Findings Na 152, K 4.1, BUN 76, Cr 2.1; Glc 116 AST/ALT: 23/47; INR 1.9 Urine tox neg; serum alc 0 Head CT: bifrontal hygromas without mass effect; old parietal encephalomalacia; basal ganglia calcification CXR: old granulomas EEG: diffuse triphasic waves
What is needed to work up confusion? Structural imaging: –Brain CT –Brain MRI Infection/hemorrhage/tumor evaluation: –Spinal tap Seizures/Brain death/psychogenic/other: –EEG Herpes Encephalitis Focal status epilepticus Other
Confusion in the Nursing Home Dementia with superimposed conditions Infection: UTI, pneumonia Medication errors/overdose End-stage medical diseases: CHF, renal Poorly managed diabetes Stroke Encephalitis/meningitis Seizure/post-ictal state Other
38 year old man Talking crazy/staggering around No recent ETHO though has a history of chronic liver disease, coagulopathy, hypertension, seizures, pancreatitis and head trauma Medications: ? Phenytoin and nadolol Exam: disheveled; 96 F; 179/100 BP; HR 112; disoriented to place, season and is confabulating with poor attention and recall; gaze-evoked nystagmus and incomplete right eye abduction on right gaze; absent reflexes and wide-based ataxic gait.
Issues Cognitive syndrome: encephalopathy Diagnosis Treatment Where is the pathology
Subtle bilateral abnormal hyperintense signal in the paraventricular region of the medial thalami seen on diffusion, flair and T2. Possible subtle abnormal signal of periaqueductal gray matter seen on flair and T2. 50 yo with mental status changes and abnormal eye movements.
Findings Subtle bilateral abnormal hyperintense signal in the paraventricular region of the medial thalami seen on diffusion, flair and T2. Possible subtle abnormal signal of periaqueductal gray matter seen on flair and T2. Further history revealed alcohol abuse. Diagnosis Wernicke's encephalopathy Discussion MRI of the brain with contrast: MRI demonstrates acute lesions of Wernicke-Korsakoff syndrome in medial thalamic and periaqueductal regions. This can be a useful diagnostic procedure in patients presenting with suggestive history and stupor or coma, where ataxia and ophthalmoplegia are not detectable. Alcohol abuse is the most common etiology. Prompt Thiamine administration is essential and actually was given to the patient prior the this MRI. Wernicke encephalopathy is a medical emergency. Prompt recognition of the symptom complex and a high index of suspicion are crucial to ensure early treatment. Early treatment can rapidly reverse the ophthalmoplegia and improve ataxia/dysequilibrium and early mental confusion, as well as prevent development of the amnestic state. In advanced cases, where severe prolonged deficiency has led to permanent structural damage, permanent deficits most often are manifested as the amnestic state and severe ataxia. Reference: emedicine. Contributor: Sanders
Chronic Alcohol Effects Cerebellar degeneration Vascular risks ICH SDH Thrombotic Embolic Seizures Cognitive Spinal cord: B12 def Neuropathy Muscular atrophy Heavy drinkers compared with light or non drinkers are: twice as likely to die of heart disease twice as likely to die of cancer twelve times as likely to die of cirrhosis of the liver three times more likely to die in a car accident six times more likely to commit suicide
60 year old man Making mistakes; forgetful; unable to complete his report; no longer interested Irritable and defensive; lost his way home Guarded/suspicious Inattentive with digit span of 5; ¼ recall & confabulates 2 others Occasional paraphasias Difficulty with 3 step command; problem with 3 D cube drawing
This 80-year-old man presented with a gradual decline in functioning. Examination revealed a marked aphasia and poor visual-spatial ability with an MMSE score of 18/30. These T1-weighted axial MR images reveal diffuse cortical atrophy with prominent sulci and enlarged lateral ventricles.
Cognitive Syndrome in the Young Differential diagnoses –Infection: HIV –Tumor –Drugs Tests
Vignette 75 year old with –Dementia –Hallucinations –Episodic alterations in consciousness –Bradykinesia Differential diagnoses
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Dementia Parkinsonism Dementia Parkinsonism Initial Symptoms AD DLBD PDD Years Later
Vignette 56 year-old with 6 month history of rapidly progressive dementia, myoclonus and increased tone
SPORADIC CJD There are three investigations which might provide support for a diagnosis of sporadic CJD. These are: The EEG The CSF estimation The MR scan Transverse FLAIR MRI showing bilateral anterior basal ganglia high signal
This is an EEG tracing showing the characteristic periodic complexes.
78 year old woman Confusion; started “talking crazy” and was stubborn Speaks with “meaningless words” and cannot answer yes/no questions accurately Can mime but cannot follow commands, name or repeat Unable to cooperate with most of exam
Questions What has happened to this woman? The nature of her deficit What mechanism? Is she aware of her deficits? In what settings is anosognosia seen? Would she be able to read aloud, write or comprehension related to reading? Visual fields would show? Discuss the Wernicke-Geschwind model of language and the anatomical localization
A = Angular Gyrus SP = Superior Parietal Lobule B = Broca’s Area T= Pars Triangularis H = Henschen’s Music Center EC = Exner’s Writing Center W = Wernicke’s Area
Definitions Aphasia: loss of the ability to use or understand language due to a brain lesion Mutism: the condition of being unable or unwilling to speak Fluency: "Production and/or perception of verbal elements of communication that adhere to the sequence, rhythm, and timing patterns approriate for the communicative context and expectations of the speaker and/or listener" (Cross, 1998). Paraphasia: A person with aphasia might use an incorrect word or unrecognizable word in place of the target word. This is a paraphasia. Paraphasias can be classified in 3 types. Phonemic or literal paraphasias are word errors that sound very close to the intended word (e.g., coke for coat). A verbal or semantic paraphasia occurs when a word that is related in meaning to the target word is substituted (e.g., plum for peach). The third type of paraphasia is a neologism - an invented word that is not recognizable as a word in the speaker's language. Dysarthria: impaired articulation due to impairment in peripheral nerves or in speech musculature Dysprosody: loss of or deficit in the comprehension or production of nonverbal aspects of language that convey attitudinal, emotional, and similar information to the listener. Apraxia: loss of the ability to produce purposeful, skilled movements as the result of brain damage
73 year old woman Sudden onset headache, dizziness with vomiting; unsteadiness of gait and poor coordination of the right arm What neurological conditions cause sudden, severe headache? What is the localizing value of dizziness, gait instability, and difficulty controlling the RUE?
Time Passes Patient is no long able to speak clearly; can open eyes and grunt Then in ER: BP 185/105; afebrile; no nuchal rigidity Extensor posturing with stimulation No response to voice and no spontaneous limb movements Pupils reactive Eyes deviate to left with cold water in left ear without nystagmus; no response when done to the right ear 2 calls –Test –Specialist
Questions What other parts of the exam is needed Eye movements? Caloric testing results in –Normal awake patient –Comatose patient with intact brainstem –Brain-dead patient Characterize and localize patient’s limb movements What is the diagnosis What phone calls were made What is the prognosis
Definitions & Underlying Structures Coma Persistent vegetative state Locked-in syndrome Brain death
Differentiate causes of Coma Diffuse processes –Findings –Causes Structural –Supratentorial –Infratentorial
Coma Exam FindingsDiencephalicMidbrainPonsMedulla Pupils: size/light response Calorics Corneals Motor response Respiration
Management How does increased intracranial pressure (ICP) cause coma? What are the treatments for increased ICP and how do they work? –Mannitol –Urea –Hyperventilation –Elevate head of bed –Steroids (for vasogenic only)
LEVELS OF CONSCIOUSNESS: Alert normal awake and responsive state Lethargic easily aroused with mild stim. Can maintain arousal. Somnolent easily aroused by voice or touch; awakens and follows commands; req stim to maintain arousal Obtunded/Stuporous arousable only with repeated and painful stim; verbal output is unintelligible or nil; some purposeful movement to noxious stim Comatose no arousal despite vigorous stim, no purposeful movement- only posturing, brainstem reflexes often absent
PUPILS: CN II afferent, CN III efferent. Tests level of the midbrain as well as autonomic integrity. Some patterns: Hypothalamus: Horner’s (miosis, ptosis, and anhydrosis) Midbrain: midpositoin, fixed Peripheral III: usually unilateral, more dilated, fixed Pons: pin point pupils Medulla (lat): Horner’s- preserved response to light Metabolic: in general met derangements do not affect pupils. The major exceptions are sympathomimetics and anti-cholinergics which dilate, and opiates which cause pin point pupils.
Other Cranial Nerves CORNEALS: V afferent, VII efferent. -pons OCULOCEPHALIC: requires levels intact from III- VIII GAG: IX, X -medulla
Check for asymmetric response as well as movement that localizes to pain, withdraws from pain, or represents posturing. Posturing: Decorticate: extension LE, flexion at elbows/wrists Better prognosis than decerebrate Often without concomitant loss neuro-optho reflexes Usually lesion is above the midbrain Decerebrate: extension LE, extension/pronation/adduction UE Often with neuro-ophtho changes Most commonly lesion at level of midbrain or di- encephalon Motor
Glasgow Coma Scale VERBAL V5 oriented V4 confused V3 inappropriate words V2 incomprehensible sounds V1 nil EYE E4 spontaneous opening E3 opens eyes to speech E2 opens eyes to noxious stim E1 nil MOTOR M6 obeys motor requests M5 localizes to noxious stim M4 withdrawal from noxious stim M3 abnormal flexion response (decorticate posturing) M2 abnormal extension (decerebrate posturing) M1 nil