1

!!Neurological and Psychological disorders

Epilepsy
Epilepsy is a disorder that is a symptom of disturbed electrical activity in the brain caused by a wide variety
of etiologies. It is a collection of many different types of seizures that vary widely in severity, appearance,
cause, consequence, and management. Epilepsy implies a periodic recurrence of seizures with or without
convulsions (sudden, violent, irregular movement of the body, caused by involuntary contraction of
muscles).
Seizures that are prolonged or repetitive can be life-threatening.

Etiology
 Seizures occur because small numbers of neurons discharge abnormally. Anything that disrupts the
normal homeostasis of the neuron and disturbs its stability may trigger abnormal activity and seizures.
A genetic predisposition to seizures has been suggested.
 Patients with mental retardation and cerebral palsy are at increased risk for seizures.
 The more profound the degree of mental retardation as measured by intelligence quotient (IQ), the
greater is the incidence of epilepsy.
 The causes of seizures in the elderly may be multifactorial and include cerebrovascular disease (both
ischemic and hemorrhagic stroke), neurodegenerative disorders, tumor, head trauma, metabolic
disorders, and CNS infections. Hyperventilation may precipitate absence seizures.
 Sleep, sleep deprivation, sensory stimuli, and emotional stress may initiate seizures.
 Hormonal changes occurring around the time of menses, puberty, or pregnancy have been associated
with the onset of or an increased frequency of seizures.
 The most clearly established risk factors for epilepsy in all age groups are head trauma (especially in
patients in whom the dura mater has been breached and in whom there is evidence of loss of
conciousness), CNS infections, and stroke.

Pathophysiology
 Seizure activity is characterized by paroxysmal discharges occurring synchronously in a large
population of cortical neurons. This is characterized on EEG as a sharp wave or spike.
 The basic physiology of a seizure episode is traceable to an unstable cell membrane or its surrounding
supportive cells. The seizure originates from the gray matter of any cortical or perhaps subcortical
area. Initially, a small number of neurons fire abnormally. Normal membrane conductances and
inhibitory synaptic currents break down, and excess excitability spreads, either locally to produce a
focal seizure or more widely to produce a generalized seizure.
 An abnormality of potassium conductance, a defect in the voltage-sensitive ion channels, or a
deficiency in the membrane ATPases linked to ion transport may result in neuronal membrane
instability and a seizure.
 Selected neurotransmitters (e.g., glutamate, aspartate, acetylcholine, norepinephrine, histamine,
corticotropin releasing factor, purines, peptides, cytokines, and steroid hormones) enhance the
excitability and propagation of neuronal activity, whereas γ -aminobutyric acid (GABA) and
dopamine inhibit neuronal activity and propagation. A relative deficiency of inhibitory
neurotransmitters such as GABA or an increase in excitatory neurotransmitters such as glutamate
would promote abnormal neuronal activity.
 Normal neuronal activity also depends on an adequate supply of glucose, oxygen, sodium, potassium,
chloride, calcium, and amino acids.
 Systemic pH is also a factor in precipitating seizures. The different kinds of epilepsies probably arise
from different neurophysiologic abnormalities.

Clinical Presentation
International Classification of Epileptic Seizures
2

I. Partial seizures (seizures begin locally)

A. Simple (without impairment of consciousness)
1. With motor symptoms
2. With special sensory or somatosensory symptoms
3. With psychic symptoms
B. Complex (with impairment of consciousness)
1. Simple partial onset followed by impairment of consciousness—with or without automatisms
2. Impaired consciousness at onset—with or without automatisms
C. Secondarily generalized (partial onset evolving to generalized tonic-clonic seizures)
II. Generalized seizures (bilaterally symmetrical and without local onset)
A. Absence
B. Myoclonic
C. Clonic
D. Tonic
E. Tonic-clonic
F. Atonic
G. Infantile spasms
III. Unclassified seizures
IV. Status epilepticus

 Partial (focal) seizures begin

in one hemisphere of the
brain and—unless they
become secondarily
generalized—result in an
asymmetric motor manifestation.
 Partial seizures manifest as alterations in motor functions, sensory or somatosensory symptoms, or
automatisms.
 Partial seizures with no loss of consciousness are classified as simple partial.
 Partial seizures with an alteration of consciousness are described as complex partial. With complex partial
seizures, the patient may have automatisms, periods of memory loss, or aberrations of behavior.
 Generalized seizures have clinical manifestations that indicate involvement of both hemispheres.
 Motor manifestations are bilateral, and there is a loss of consciousness. Generalized seizures may be further
subdivided by EEG and clinical manifestations.
 Generalized absence seizures are manifested by a sudden onset, interruption of ongoing activities, a blank
stare, and possibly a brief upward rotation of the eyes.
 GTC seizures results in a sudden sharp tonic contraction of muscles followed by a period of rigidity and
clonic movements. During the seizure, the patient may cry or moan, lose sphincter control, bite the tongue, or
develop cyanosis.
 After the seizure, the
patient may have altered
consciousness,
drowsiness, or confusion
for a variable period of
time (postictal period) and
frequently goes into a deep
sleep. Tonic and clonic
seizures may occur
3

separately.
 Brief shocklike muscular contractions of the face, trunk, and extremities are known as myoclonic jerks.
 They may be isolated events or rapidly repetitive. A sudden loss of muscle tone is known as an atonic seizure.
This may be described as a head drop, the dropping of a limb, or a slumping to the ground. These patients
often wear protective headware to prevent trauma.
 Status epilepticus (SE) is a common neurologic emergency that may be associated with brain damage and
death. SE is (1) any seizure lasting longer than 30 minutes whether or not consciousness is impaired or (2)
recurrent seizures without an intervening period of consciousness between 3 seizures.
Symptoms
 Symptoms of a specific seizure will depend on seizure type. While seizures can vary between patients, they
tend to be stereotyped within an individual.
 Complex partial seizures may include somatosensory or focal motor features. Complex partial seizures are
associated with altered consciousness.
 Absence seizures may appear relatively bland, with only very brief (seconds) periods of altered consciousness.
 Generalized tonic-clonic seizures are major convulsive episodes and are always associated with a loss of
conciousness.
Signs
Interictally (between seizure episodes), there are typically neither objective nor pathognomonic signs of epilepsy.

Other Diagnostic Tests

EEG is very useful in the diagnosis of various seizure disorders. The EEG may be normal in some patients
who still have the clinical diagnosis of epilepsy.
While MRI is very useful (especially imaging of the temporal lobes), CT scan typically is not helpful except in
the initial evaluation for a brain tumor or cerebral bleeding.

Parkinson Disease
Parkinsonism is a clinical syndrome characterized by diminished facial expression, stooped posture, slowness
of voluntary movement, festinating gait (progressively shortened, accelerated steps), rigidity, and a
“pill-rolling” tremor.
Etiology: Exact etiology is not known but some of the risk factors are listed: Pesticide exposure, Drugs that
have neurological effects or Familial history
Pathogenesis: No unifying pathogenic mechanism has emerged yet many possibilities have been suggested,
including a misfolded proteins, defective proteosomal function and altered mitochondrial function.
Pathophysiology: The dopaminergic neurons of the substantia nigra project to the striatum, and their
degeneration in PD is associated with a reduction in the striatal dopamine content. The severity of the motor
response related clinical features is proportional to the dopamine deficiency.
Morphology and Microscopy
The typical macroscopic findings are Pallor (unhealthy pale appearance) of the substantia nigra and locus
ceruleus.

Figure A&B: Normal and depigmented SN in PD, FigureC: Lewy body in a substantia nigra neuron, (arrow)
4

On microscopic examination, there is loss of the pigmented, catecholaminergic neurons in SN region,

associated with gliosis. Lewy bodies may be found in some of the remaining neurons of SN.

Clinical Features and Complications:

 In addition to the signs of Parkinsonism, autonomic dysfunction is common, as is some impairment of
cognitive function. Parkinson disease is sometimes accompanied by a dementia, either early in the course of
the illness or as a late additional morbidity.

Stroke
Definition: World Health Organization defined stroke as a "neurological deficit of cerebrovascular cause
that persists beyond 24 hours or is interrupted by death within 24 hours“
The 24-hour limit divides stroke from transient ischemic attack, (TIA) which is a related syndrome of
stroke symptoms that resolve completely within 24 hours.
It can be considered as an event because of -
Hypoxia, ischemia, and infarction resulting from impairment of blood supply and oxygenation of CNS
tissue (Ischemic stroke)
Hemorrhage resulting from rupture of CNS vessels (Haemorrhagic)

Ischemic stroke

Cessation of blood flow can result from a reduction in perfusion pressure (as in hypotension), small- or
large-vessel obstruction, or both.
Causes of Cerebral ischemia
 Thrombosis (obstruction of a blood vessel by a blood clot forming locally)
 Embolism (obstruction due to an embolus from elsewhere in the body),
 Systemic hypoperfusion (general decrease in blood supply, e.g., in shock)
 Cerebral venous sinus thrombosis

The duration of ischemia, and the magnitude and rapidity of the reduction of flow determines, in turn, the
precise anatomic site and size of the lesion and, consequently, the clinical deficit. Two principal types of
acute ischemic injury are recognized:
Global cerebral ischemia (ischemic/hypoxic encephalopathy) occurs when there is a generalized reduction
of cerebral perfusion, as in cardiac arrest, shock, and severe hypotension.
Focal cerebral ischemia follows reduction or cessation of blood flow to a localized area of the brain due to
large vessel disease (such as embolic or thrombotic arterial occlusion, often in a setting of atherosclerosis)
or to small-vessel disease (such as vasculitis or occlusion secondary to arteriosclerotic lesions seen in
hypertension).
A stroke without an obvious explanation is termed cryptogenic (of unknown origin)

There are a number of factors that can increase your risk of having a cerebellar stroke. Risk factors that
5

could lead to a blood clot or obstruction include:

 smoking  diabetes
 high cholesterol  high blood pressure
 obesity  atherosclerosis, or a narrowing of the arteries
 physical inactivity  heart disease
Pathophysiology
Ischemic stroke occurs because of a loss of blood supply to part of the brain, due to atherosclerosis in
arteries responsible for cerebral circulation. This blockade may be due the formation of blood clots within
the vessel, or by releasing showers of small emboli through the disintegration of atherosclerotic
plaques. As oxygen or glucose becomes depleted in ischemic brain tissue, the production of high energy
phosphate compounds such as adenosine triphosphate (ATP) fails, leading to failure of energy-dependent
processes (such as ion pumping) necessary for tissue cell survival. This sets off a series of interrelated
events that result in cellular injury and death. Brain tissue ceases to function if deprived of oxygen for more
than 60 to 90 seconds, and after approximately three hours will suffer irreversible injury possibly leading to
the death of the tissue, i.e., infarction.

Hemorrhagic stroke

Hemorrhagic strokes are classified based on their underlying pathology. Some causes of hemorrhagic stroke
are hypertensive hemorrhage, ruptured aneurysm, ruptured AV fistula (abnormal connection between artery
and vein), transformation of prior ischemic infarction, and drug induced bleeding. They result in tissue
injury by causing compression of tissue from an expanding hematoma or hematomas. In addition, the
pressure may lead to a loss of blood supply to affected tissue with resulting infarction, and the blood
released by brain hemorrhage appears to have direct toxic effects on brain tissue and vasculature.
Stroke symptoms typically start suddenly, over seconds to minutes, and in most cases do not progress
further. The symptoms depend on the area of the brain affected. The more extensive the area of the brain
affected, the more functions that are likely to be lost.
Signs and Symptoms: Common symptoms of a cerebral stroke include:
 dizziness  vomiting
 headaches  double vision
 nausea  tremors
More visible symptoms of a cerebellar stroke may include:
 vertigo  difficulty speaking or slurred speech
 poor coordination  uncontrollable eye movement
 abnormal reflexes  unconsciousness
 difficulty swallowing


DEPRESSION
 Depression is a mood disorder characterized by persistently low mood and a feeling of sadness and loss
of interest. It is a persistent problem, not a passing one, lasting on average 6 to 8 months.
6

 It’s a common but serious disease that can take away a person’s ability to enjoy life and cause decline in
capacity to undertake even the simplest daily tasks. Other than its chronic nature, symptoms associated
with this mental disorder are often recurring and life threatening.
 There are indeed diverse forms of depression that can either be mild or extremely severe conditions like
psychotic depression in which the patients show symptoms such as hallucinations and delusions.
 Major depressive disorder: Patients with major depressive disorder typically show dysphoric mood and
anhedonia accompanied by physical changes such as weight loss or gain, increased or decreased appetite,
alteration in sleep pattern and sustained fatigue. Disturbances in cognitive and executive functions are
also manifested by lack of concentration and coherent thinking as well as morbid preoccupation by
thoughts of death and suicide. Majority of these symptoms normally are present nearly every day and
result in significant distress and impaired social life and occupational performance.
 Dysthymic disorder:It is also known as persistent depressive disorder. Patients display depressed mood
or sadness that persists for the majority of the duration of the day for a minimum of two years in adults
and one year in children and adolescents. Majority of the patients do not meet the full criteria for MDD as
there is interruption by short periods of remission. However, there are instances where patients meet full
criteria in which they are diagnosed with MDD.
 Melancholic depression: There is an almost absolute lack of ability to experience pleasure. Psychomotor
retardation and early morning worsening of mood is also apparent in this subset of patients. This type of
depression is seen more commonly in the elderly, in patients with more severe forms of depression and
psychotic depression
 Seasonal affective disorder (SAD): It is a type of depression described as recurring annually during fall
or early winter. This ‘winter blues’ or SAD is characterized by low mood, feelings of guilt and
worthlessness and increased irritability, symptoms shared with other depressive disorders. Additionally,
patients show a significant increase in appetite and craving for foods high in carbohydrates which result
in weight gain.
 Post-partum depression (PPD): This describes a heterogeneous group of depressive symptoms that
affects mothers. These symptoms may surface before or after giving birth. Half of the “postpartum”
episodes begin before the time of delivery. Thus, are referred to collectively as “peri-partum” episodes.
 Psychotic depression: is a type of depressive disorder which is very severe and accompanied by
psychotic symptoms. It is commonly seen as a combination of psychosis and depression that is not
separable into either of the two. Symptoms include psychotic features such as hallucinations or
delusions. Other than its severity psychotic depression is associated with prolonged course, poor
response to available drugs and higher relapse rate
 Pathophysiology of depression
There are diverse theories on the pathogenesis of depression most based on measurement of indirect
markers, post-mortem studies and neuro-imaging techniques.
A) Neural circuitry of depression: Various structural and functional studies report abnormalities in the areas
of the brain that are responsible for the regulation of mood, reward response and executive functions.
Post-mortem and neuro-imaging studies have reported morphological changes indicated by reductions in
grey-matter volume and glial density in the prefrontal cortex and the hippocampus, regions that have
received the most attention in animal research on depression.
The mesolimbic dopamine system that consists of the nucleus accumbens (NAc) and the ventral tegmental
area (VTA) also are believed to play a role in the pathogenesis of depression.
B) Stress response circuits: Chronic stress and hyperactivity of the HPA axis (causing chronic
hypercortisolemia) have been hypothesized to play a prominent role in the incidence of depression and even
in recurrence after complete remission. One of the brain structures affected is the amygdala, area of the
brain involved in mainly regulating emotional reactivity and to some degree stress response.
C) Genetic vulnerability and environmental interaction: The rate-limiting enzyme in serotonin
biosynthesis, tryptophan hydroxylase (TPH), is encoded by two distinct genes Tphl and Tph2 and has been
7

proposed to play a role in pathogenesis of depressive disorders and suicide. Single nucleotide
polymorphisms (SNPs) on Tph2 gene have been linked with increased incidence of MDD and completed
suicide attempts.
D) The biogenic monoamine theory:
i) The Serotonin hypothesis: Serotonin is a monoamine neurotransmitter with a wide range distribution
throughout the central nervous system. It is involved in physiologic activities such as pain sensation,
appetite regulation, aggression and mood. Dysfunction in serotonergic system has been implicated in mood
and anxiety disorders.
ii) The catecholamine hypothesis: Some symptoms of depression including anhedonia and psychomotor
retardation are better explained by a derangement in the brain DA systems. These systems include the
substantia nigra -basal ganglia motor system and the reward circuitry involving the NAc and VTA. There is
a diminished DA activity in the NAc specifically which corresponds to the inability to experience pleasure
which is one of the hallmarks of depression.

E) Inflammation and depression:

Many pro-inflammatory marker levels are reported to be elevated in depressed patients. Examples of these
markers are C-reactive protein (CRP), interleukin (IL)-6, IL-1 and tumor necrosis factor alpha (TNF-α). In
fact depressive like behaviors can be induced in the laboratory by administration of (IFN)-α, a powerful
inflammatory cytokine, that has also been shown to produce depression like symptoms in patients taking it
for the treatment of hepatitis C.
F) Neuropeptides and depression: There is increasing evidence that this neuropeptides are involved in the
modulation of stress- related behaviors and mood by acting on neurokinin type-1 receptors (NK1).
Substance P (SP) is one of these neuropeptides known for its wide spread distribution in the brain and its
co-localization with 5-HT and NE neurons. Elevated CSF SP concentrations have been reported in
depressed patients and patients with post traumatic stress disorder after exposure to a stressful stimulus.
G) Hormones and depression
i. Thyroid hormones: Thyroid hormones (TH) imbalances are implicated in the pathophysiology of
neurodegenerative and psychiatric conditions. These hormones are very essential for brain development,
maturation and have been shown to promote neurogenesis, in particular, in the hippocampus.
Hypothyroidism has been linked to depressive -like behavior in that it impaired hippocampal neurogenesis
which resolved with hormone replacement.
Estrogen enhances mood by increasing the rate of degradation of MAO and intraneuronal 5- HT transport,
causing an overall increase in 5-HT availability in the synapse. In addition serotonergic neurotransmission,
estrogen also is believed to have modulatory effect on hippocampal neurogenesis, BDNF signaling, and
HPA axis function.
iii. Vasopressin and depression: Arginine vasopressin (AVP) is a hypothalamic hormone that influences
8

some key symptoms pertinent to major depressive disorder. Its level is reported to be elevated in patients
suffering from this mental disorder.
iv. Delayed circadian rhythm in patients with depression has been linked to diminished level of
melatonergic signaling in the brain. Patients may manifest with delayed onset of sleep, difficulty in
maintaining sleep and early morning awakening.

Schizophrenia
 Schizophrenia is a chronic and severe mental disorder that affects how a person thinks, feels, and
behaves. People with schizophrenia may seem like they have lost touch with reality.
 Schizophrenia is characterised by thoughts or experiences that seem out of touch with reality,
disorganised speech or behaviour and decreased participation in daily activities. Difficulty with
concentration and memory may also be present.
 Etiology: Schizophrenia has its origins in some as yet unknown in utero disturbance, possibly occurring
during the second trimester of pregnancy. Evidence for this is provided by the abnormal neuronal
migration demonstrated in most studies of schizophrenic brains.
 This “schizophrenic lesion” may result in abnormalities in cell shape, position, symmetry, and
connectivity, and functionally to the development of abnormal brain circuits.
 Changes are consistent with a cell migration abnormality during the second trimester of pregnancy, and
some studies associate upper respiratory infections during the second trimester of pregnancy with a
higher incidence of schizophrenia.
 Additional support for a developmental model is provided by the fact that although studies have shown
decreased cortical thickness and increased ventricular size in the brains of many patients with
schizophrenia, this occurs in the absence of widespread gliosis.
 Gliosis, or the proliferation of glial cells, is thought to occur as a compensatory change in degenerative
diseases of the brain.
 Obstetric complications and hypoxia, in combination with a genetic predisposition, could activate a
glutamatergic cascade that results in increased neuronal pruning.
 Neuropsychological abnormalities as early as 4 years of age in individuals who later develop
schizophrenia.
 Impairment in reaching normal motor milestones, and abnormal movements in children as young as 8
months of age, have been associated with the development of schizophrenia.
 Pathophysiology: Computed axial tomography (CAT) scans and magnetic resonance imaging (MRI)
studies show increased ventricular size, particularly in the third and lateral ventricles. There is a small
but definite decrease in brain size as compared to matched controls.
 These changes appear to be consistent with brain asymmetry, the ventricular enlargement being most
pronounced in the left temporal horn, and the decreased cortical size being most obvious in the left
temporal lobe.
9
10

A. Characteristic symptoms: Two or more of the following, each persisting for a significant portion of at least a
1-month period:
(1) delusions
(2) hallucinations
(3) disorganized speech
(4) grossly disorganized or catatonic behavior
(5) negative symptoms
Note: Only one criterion A symptom is required if delusions are bizarre or if hallucinations consist of a voice
keeping a running commentary on the person’s behavior or two or more voices conversing with each other.
B. Social/occupational dysfunction: For a significant portion of the time since onset of the disorder, one or more
major areas of functioning such as work, interpersonal relations, or self-care are significantly below the level
prior to onset.
C. Duration: Continuous signs of the disorder for at least 6 months. This must include at least 1 month of
symptoms fulfilling criterion A (unless successfully treated). This 6 months may include prodromal or residual
symptoms.
D. Schizoaffective or mood disorder has been excluded.
E. Disorder is not due to a medical disorder or substance use.
F. If a history of a pervasive developmental disorder is present, there must be symptoms of hallucinations or
delusions present for at least 1 month.

Alzheimer's disease
Alzheimer's disease (AD), also referred to simply as Alzheimer's, is a chronic neurodegenerative disease that
usually starts slowly and worsens over time. It is the cause of 60–70% of cases of dementia. The most common
early symptom is difficulty in remembering recent events (short-term memory loss).
The exact etiology of AD is unknown; however, several genetic and environmental causes have been explored as
potential causes of AD.
Genetic factors have been investigated in both early- and late onset AD. Almost all early-onset cases of AD can
be attributed to alterations on chromosomes 1, 14, or 21. The majority and most aggressive early-onset cases are
attributed to mutations of an Alzheimer’s gene located on chromosome 14.
A number of environmental factors have been associated with an increased risk of AD, including stroke, alcohol
abuse, small head circumference, repeated or severe head trauma, Down syndrome, and lower levels of
11

education.
Pathophysiology:
Structural changes: AD is defined by both neuropathologic and clinical criteria. Neuropathologically, AD
destroys neurons in the cortex and limbic structures of the brain, particularly the basal forebrain, amygdala,
hippocampus, and cerebral cortex. These areas are responsible for higher learning, memory, reasoning,
behavior, and emotional control.

Anatomically, four major alterations in brain structure are seen: cortical atrophy, degeneration of
cholinergic and other neurons, presence of neurofibrillary tangles (NFTs), and the accumulation of neuritic
plaques. NFTs and neuritic plaques are considered the signature lesions of AD; without them ADdoes not
occur.

Microglial cells located around and within amyloid plaques are thought to release inflammatory mediators,
which locally destroy neuronal tissue. Glial cells also function as phagocytes, similar to macrophages and
monocytes in the periphery.
 Multiple neuronal pathways are destroyed in AD. Most profoundly damaged are the cholinergic
pathways, particularly a large system of neurons located at the base of the forebrain, a brain area believed
to be involved in thought integration. Serotonergic neurons of the raphe nuclei and noradrenergic cells of
the locus ceruleus are lost.
 Glutamate and other excitatory amino acid neurotransmitters have been implicated as potential
neurotoxins in AD. If glutamate is allowed to remain in the synapse for extended periods of time, it can
destroy nerve cells.
 The elevated cholesterol levels in brain neurons may alter membrane functioning and result in the
12

cascade leading to plaque formation and AD.

 Estrogen is thought to be involved in promoting neuronal growth, and in preventing oxidative damage,
which would benefit cells exposed
 to βAP. Estrogen receptors are present in the brain, and are distributed in a pattern consistent with areas
destroyed in AD.
Clinical signs and symptoms:
 Cognitive: Memory loss (poor recall and losing items); aphasia (circumlocution and anomia); apraxia;
agnosia; disorientation (impaired perception of time and unable to recognize familiar people); impaired
executive function
 Noncognitive: Depression, psychotic symptoms (hallucinations and delusions), behavioral disturbances
(physical and verbal aggression, motor hyperactivity, uncooperativeness, wandering, repetitive
mannerisms and activities, and combativeness) Functional: Inability to care for self (dressing, bathing,
toileting, and eating)
Stages of Schizophrenia
 Stage 1 Normal: No subjective or objective change in intellectual functioning.
 Stage 2 Forgetfulness: Complaints of losing things or forgetting names of acquaintances. Does not
interfere with job or social functioning. Generally a component of normal aging.
 Stage 3 Early confusion: Cognitive decline causes interference with work and social functioning.
Anomia, difficulty remembering right word in conversation, and recall difficulties are present and
noticed by family members. Memory loss may cause anxiety for patient.
 Stage 4 Late confusion (early AD): Patient can no longer manage finances or homemaking activities.
Difficulty remembering recent events. Begins to withdraw from difficult tasks and to give up hobbies.
May deny memory problems.
 Stage 5 Early dementia (moderate AD) : Patient can no longer survive without assistance. Frequently
disoriented with regard to time (date, year, season). Difficulty selecting clothing. Recall for recent events
is severely impaired; may forget some details of past life (e.g., school attended or occupation).
Functioning may fluctuate from day to day. Patient generally denies problems. May become suspicious
or tearful. Loses ability to drive safely.
 Stage 6 Middle dementia (moderately severe AD): Patients need assistance with activities of daily living
(e.g., bathing, dressing, and toileting). Patients experience difficulty interpreting their surroundings; may
forget names of family and caregivers; forget most details of past life; have difficulty counting backward
from 10. Agitation, paranoia, and delusions are common.
 Stage 7 Late dementia: Patient loses ability to speak (may only grunt or scream), walk, and feed self.
Incontinent of urine and feces. Consciousness reduced to stupor or coma.