Blueprints Psychiatry 6th Edition Ebook PDF
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Contributors
Preface
Acknowledgments
Abbreviations
1 Psychotic Disorders
2 Bipolar Disorders
3 Depressive Disorders
4 Anxiety Disorders
7 Eating Disorders
10 Substance-Related Disorders
11 Personality Disorders
12 Miscellaneous Disorders
14 Legal Issues
15 Antipsychotics
17 Mood Stabilizers
18 Anxiolytics
19 Miscellaneous Medications
Questions
Answers
Appendix
Index
Margaret Benningfield, MD
Assistant Professor of Psychiatry and Behavioral Sciences
Department of Psychiatry and Behavioral Sciences
Vanderbilt University School of Medicine
Nashville, Tennessee
Sheryl Fleisch, MD
Assistant Professor of Psychiatry and Behavioral Sciences
Department of Psychiatry and Behavioral Sciences
Vanderbilt University School of Medicine
Nashville, Tennessee
Bradley Freeman, MD
Associate Professor of Clinical Psychiatry and Behavioral Sciences
Department of Psychiatry and Behavioral Sciences
Vanderbilt University School of Medicine
Nashville, Tennessee
Meghan Riddle, MD
Assistant Professor of Psychiatry and Behavioral Sciences
Department of Psychiatry and Behavioral Sciences
Vanderbilt University School of Medicine
Nashville, Tennessee
Lloyd I. Sederer, MD
Chief Medical Officer
New York State Office of Mental Health
Adjunct Professor
Columbia/Mailman School of Public Health
Medical Editor for Mental Health
The Huffington Post
Contributing Writer
US News and World Report
New York, New York
Maja Skikic, MD
Assistant Professor of Psychiatry and Behavioral Sciences
Department of Psychiatry and Behavioral Sciences
Vanderbilt University School of Medicine
Nashville, Tennessee
Jonathan Smith, MD
Fellow in Consultation-Liaison Psychiatry
Department of Psychiatry and Behavioral Sciences
Vanderbilt University School of Medicine
Nashville, Tennessee
Edwin Williamson, MD
Assistant Professor of Psychiatry and Behavioral Sciences
Department of Psychiatry and Behavioral Sciences
Vanderbilt University School of Medicine
Nashville, Tennessee
lueprints Psychiatry was conceived by a group of recent
B medical school graduates who saw that there was a need for a
thorough yet compact review of psychiatry that would adequately
prepare students for the USMLE yet would be digestible in small
pieces that busy residents can read during rare moments of calm
between busy hospital and clinical responsibilities. Many students
have reported that the book is also useful for the successful
completion of the core and advanced psychiatry clerkships. We
believe that the book provides a good overview of the field that the
student should supplement with more in-depth reading. Before
Blueprints Psychiatry, we felt that review books were either too
cursory to be adequate or too detailed in their coverage for busy
readers with little free time. We have kept the content current by
repeated updates and revisions of the book while retaining a
balance between comprehensiveness and brevity. This new edition
reflects changes in response to user feedback. The structure of the
book mirrors the major concepts and therapeutics of modern
psychiatric practice. We cover each major diagnostic category,
each major class of somatic and psychotherapeutic treatment, legal
issues, and special situations that are unique to the field. In this
edition, we have updated all diagnoses to those included in the
current Diagnostic and Statistical Manual, 5th edition (DSM-5) and
have included new images, 25% more USMLE study questions,
and a Neural Basis section for each major diagnostic category. We
recommend that those preparing for USMLE read the book in
chapter order but cross reference when helpful between diagnostic
and treatment chapters. We hope that Blueprints Psychiatry fits as
neatly into your study regimen as it fits into your backpack or
briefcase. You never know when you’ll have a free moment to
review for the boards!
Michael J. Murphy
Ronald L. Cowan
e would like to acknowledge the faculty, staff, medical
W students, and trainees of the Vanderbilt Psychiatric Hospital
and Vanderbilt University Medical Center for their contributions
and ongoing inspiration.
Michael J. Murphy
Ronald L. Cowan
AA Alcoholics anonymous
ABG Arterial blood gas
ACLS Advanced cardiac life support
ADHD Attention-deficit/hyperactivity disorder
ASP Antisocial personality disorder
BAL Blood alcohol level
BID Twice daily
CBC Complete blood count
CBT Cognitive-behavioral therapy
CNS Central nervous system
CO2 Carbon dioxide
CPR Cardiopulmonary resuscitation
CSF Cerebrospinal fluid
CT Computerized tomography
CVA Cerebrovascular accident
DBT Dialectical behavior therapy
DID Dissociative identity disorder
DT Delirium tremens
ECG Electrocardiogram
ECT Electroconvulsive therapy
EEG Electroencephalogram
EPS Extrapyramidal symptoms
EW Emergency ward
FBI Federal Bureau of Investigation
5HIAA 5-hydroxy indoleacetic acid
5HT 5-hydroxy tryptamine
GABA Gamma-amino butyric acid
GAD Generalized anxiety disorder
GHB Gamma-hydroxybutyrate
GI Gastrointestinal
HIV Human immunodeficiency virus
HPF High-power field
ICU Intensive care unit
IM Intramuscular
IPT Intrapersonal therapy
IQ Intelligence quotient
IV Intravenous
LP Lumbar puncture
LSD Lysergic acid diethylamine
MAOI Monoamine oxidase inhibitor
MCV Mean corpuscular volume
MDMA 3,4-methylenedioxy-methamphetamine
MR Mental retardation
MRI Magnetic resonance imaging
NIDA National Institute on Drug Abuse
NMS Neuroleptic malignant syndrome
OCD Obsessive-compulsive disorder
PCA Patient-controlled analgesia
PMN Polymorphonuclear leukocytes
PO By mouth
PTSD Posttraumatic stress disorder
QD Each day
REM Rapid eye movement
SES Socioeconomic status
SSRI Selective serotonin reuptake inhibitor
TCA Tricyclic antidepressant
TD Tardive dyskinesia
T4 Tetra-iodo thyronine
TID Three times daily
TSH Thyroid-stimulating hormone
T3 Tri-iodo thyronine
WBC White blood cell count
WISC-R Wechsler Intelligence Scale for Children–Revised
Psychotic disorders are a collection of disorders in which
psychosis, defined as a gross impairment in reality testing,
predominates the symptom complex. Psychotic symptoms are
characterized into five domains: hallucinations, delusions,
disorganized thought, disorganized or abnormal motor behavior,
and negative symptoms. Table 1-1 lists the Diagnostic and
Statistical Manual of Mental Disorders, Fifth edition (DSM-5)
classification of the psychotic disorders.
NEURAL BASIS
Much of our understanding of the neural basis for psychotic
disorders is based in research on schizophrenia. Schizophrenia is
currently considered a neurodevelopmental illness. Reduced
regional brain volume with enlarged cerebral ventricles is a
hallmark finding. Brain volume is reduced in limbic regions
including amygdala, hippocampus, and parahippocampal gyrus.
The prefrontal cortex microanatomy is altered. Thalamic and basal
ganglia regions are also affected. Altered dopamine function is
strongly implicated in positive and negative symptoms of
schizophrenia. An excess of dopamine in the mesolimbic pathway
is thought to contribute to the positive symptoms of schizophrenia,
whereas deficient dopamine function in the mesocortical pathways
is thought to contribute to the negative symptoms. γ-Aminobutyric
acid (GABA), glutamate, and the other monoamine
neurotransmitters are also likely affected.
SCHIZOPHRENIA
Schizophrenia is a disorder in which patients have psychotic
symptoms and social or occupational dysfunction that persists for
at least 6 months.
EPIDEMIOLOGY
Schizophrenia affects 1% of the population. The typical age of
onset is the late teens to the early 20s for men and the mid- to late
20s for women. Women are more likely to have a “first break” later
in life; in fact, about one-third of women have an onset of illness
after age 30, with a second peak occurring after menopause.
Schizophrenia is diagnosed disproportionately among the lower
socioeconomic classes; although theories exist for this finding,
none has been substantiated.
RISK FACTORS
Risk factors for schizophrenia include genetic risk factors (family
history), prenatal and perinatal factors such as difficulties or
infections during maternal pregnancy or delivery, winter births,
neurocognitive abnormalities such as low premorbid intelligence
quotient (IQ) or early childhood neurodevelopmental difficulties,
urban living, migration to a different culture, sexual trauma, and
cannabis use (especially in susceptible individuals).
ETIOLOGY
The etiology of schizophrenia is unknown. There is a clear
inheritable component, but familial incidence is sporadic, and
schizophrenia does occur in families with no history of the disease.
Schizophrenia is widely believed to be a neurodevelopmental
disorder. Multiple neuronal types and pathways appear to be
implicated, including those using the neurotransmitters dopamine,
glutamate, and GABA.
Dopamine
The most widely investigated theory for contributions to
schizophrenia is the dopamine hypothesis, which posits that
schizophrenia is due to hyperactivity in brain dopaminergic
pathways. This theory is consistent with the efficacy of
antipsychotics (which block dopamine receptors) (Fig. 1-1) and the
ability of drugs (such as cocaine or amphetamines) that stimulate
dopaminergic activity to induce psychosis. Postmortem studies
have also shown higher numbers of dopamine receptors in specific
subcortical nuclei of those with schizophrenia than in those with
normal brains.
FIGURE 1-2. Glutamate: The drug phencyclidine (PCP) can block the
N-methyl-d-aspartate (NMDA) receptor channel and is associated with
hallucinations and paranoia in humans. Similarly, autoimmune
reactions against the NMDA receptor (known as anti-NMDA receptor
encephalitis) can produce a range of psychotic symptoms. (From Bear
MF, Connors BW, Paradiso MA. Neuroscience: Exploring the Brain,
4th ed. Philadelphia, PA: Wolters Kluwer, 2015.)
γ-Aminobutyric Acid
Alterations in prefrontal cortical GABA interneurons are most
strongly linked to cognitive impairments in schizophrenia. There
do not appear to be reductions in overall GABA interneurons in the
prefrontal cortex but the synthetic enzyme (GAD67) for GABA is
lower in a subset of these neurons, among other indicators of
altered GABA function such as altered GABA reuptake.
More recent studies have focused on structural and functional
abnormalities through brain imaging of patients with schizophrenia
and control populations. No one finding or theory to date suffices
to explain the etiology and pathogenesis of this complex disease.
CLINICAL MANIFESTATIONS
Diagnostic Evaluation
The diagnostic evaluation for schizophrenia involves a detailed
history, physical, and laboratory examination, preferably including
brain magnetic resonance imaging (MRI). Although there is no
diagnostic laboratory or imaging finding for schizophrenia,
cerebral ventricular enlargement is typical. Medical causes, such as
neuroendocrine abnormalities and psychostimulant use disorder,
and such brain insults as tumors or infection, should be ruled out.
DIFFERENTIAL DIAGNOSIS
The differential diagnosis of an acute psychotic episode is broad
and challenging (Table 1-4). Once a medical or substance-related
condition has been ruled out, the task is to differentiate
schizophrenia from a schizoaffective disorder, a mood disorder
with psychotic features, a delusional disorder, or a personality
disorder.
Hypoxic
encephalopathy
Metabolic Causes
Acute intermittent Hypo- and hypercalcemia
porphyria
Cushing’s syndrome Hypo- and hyperthyroidism
Early hepatic Paraneoplastic syndromes (anti-NMDA [N-
encephalopathy methyl d-aspartate] receptor encephalitis;
limbic encephalitis)
Nutritional Causes
Niacin deficiency Vitamin B12 deficiency
(pellagra)
Thiamine deficiency
(Wernicke-Korsakoff’s
syndrome)
From Rosenbaum JF, Arana GW, Hyman SE, et al. Handbook of Psychiatric Drug Therapy, 5th ed.
Philadelphia, PA: Lippincott Williams & Wilkins, 2005.
MANAGEMENT
Antipsychotic agents are primarily used in treatment. These
medications are used to treat acute psychotic episodes and to
maintain patients in remission or with long-term illness.
Antipsychotic medications are discussed in Chapter 15.
Combinations of several classes of medications are often
prescribed in severe or refractory cases. Psychosocial treatments,
including stable reality-oriented psychotherapy with increasing
support for cognitive behavioral therapy, family support,
psychoeducation, social and vocational skills training, and attention
to details of living situation (housing, roommates, daily activities)
are critical to the long-term management of these patients.
Complications of schizophrenia include those related to
antipsychotic medications, secondary consequences of poor health
care and impaired ability to care for oneself, and increased rates of
suicide. Once diagnosed, schizophrenia is a long-term
remitting/relapsing disorder with impaired interepisode function.
Poorer prognosis occurs with early onset, a history of head trauma,
or comorbid substance abuse.
SCHIZOAFFECTIVE DISORDER
Patients with schizoaffective disorder have psychotic episodes that
resemble schizophrenia but with prominent mood
disturbances. Their psychotic symptoms, however, must persist
for at least 2 weeks in the absence of any mood syndrome.
EPIDEMIOLOGY
Lifetime prevalence is estimated at 0.5% to 0.8%. Age of onset is
similar to schizophrenia (late teens to early 20s).
RISK FACTORS
Risk factors for schizoaffective disorder are not well established
but likely overlap with those of schizophrenia and affective
disorders.
ETIOLOGY
The etiology of schizoaffective disorder is unknown. It may be a
variant of schizophrenia, a variant of a mood disorder, a distinct
psychotic syndrome, or simply a superimposed mood disorder and
psychotic disorder.
CLINICAL MANIFESTATIONS
Diagnostic Evaluation
The diagnostic evaluation for schizoaffective disorder is similar to
other psychiatric conditions and involves a detailed history,
physical, and laboratory examination, preferably including brain
magnetic resonance imaging. Medical conditions producing
secondary behavioral symptoms should be ruled out.
DIFFERENTIAL DIAGNOSIS
Mood disorders (depressive or bipolar disorders) with psychotic
features, as in mania or psychotic depression, are different from
schizoaffective disorder in that patients with schizoaffective
disorder have persistence (for at least 2 weeks) of the psychotic
symptoms after the mood symptoms have resolved. Schizophrenia
is differentiated from schizoaffective disorder by the absence of a
prominent mood disorder in the course of the illness.
It is important to distinguish the prominent negative symptoms
of the patient with schizophrenia from the lack of energy or
anhedonia in the depressed patient with schizoaffective disorder.
More distinct symptoms of a mood disturbance (such as depressed
mood and sleep disturbance) should indicate a true coincident
mood disturbance.
MANAGEMENT
Patients are treated with medications that target the psychosis and
the mood disorder. Typically, these patients require the
combination of an antipsychotic medication and a mood
stabilizer. Mood stabilizers are described in Chapter 17. An
antidepressant or electroconvulsive therapy may be needed for an
acute depressive episode. Psychosocial treatments are similar for
schizoaffective disorder and schizophrenia. Complications of
schizoaffective disorder include those related to antipsychotic and
mood stabilizer medications, secondary consequences of poor
health care and impaired ability to care for oneself, and increased
rates of suicide. Prognosis is better than for schizophrenia and
worse than for bipolar disorder or major depression. Patients with
schizoaffective disorder are more likely than those with
schizophrenia but less likely than mood-disordered patients to have
a remission after treatment.
SCHIZOPHRENIFORM DISORDER
Essentially, schizophreniform disorder is diagnosed when an
individual has symptoms of schizophrenia that last between 1 and 6
months. The diagnostic criteria do not require the presence of
impaired social or occupational functioning, although they can be
present.
EPIDEMIOLOGY
Outcome studies of this disorder indicate that about one-third of the
patients recover but most of the remaining two-thirds are ultimately
diagnosed with schizophrenia or schizoaffective disorder. The
diagnosis of schizophreniform disorder may help avoid premature
diagnosis of patients with schizophrenia before some other
disorder, such as bipolar disorder, manifests itself.
RISK FACTORS
Because most patients with schizophreniform disorder are
eventually diagnosed with schizophrenia, risk factors are likely
similar for the two groups.
ETIOLOGY
At this time, the etiology is unknown. At least one study found
similarities in brain structure abnormalities between patients with
schizophrenia and those with schizophreniform disorder.
CLINICAL MANIFESTATIONS
MANAGEMENT
The disorder is by definition self-limited. When symptoms cause
severe impairment, treatment is similar to that for the acute
treatment of psychosis in schizophrenia.
EPIDEMIOLOGY
This condition is twice as common in females. The average onset is
in ones in their mid-30s.
ETIOLOGY
Although the etiology is unknown, the disorder seems to be
associated with borderline personality disorder and schizotypal
personality disorder.
CLINICAL MANIFESTATIONS
DIFFERENTIAL DIAGNOSIS
It is important to rule out schizophrenia, especially if the disorder
worsens or persists for more than a month. A mood disorder such
as mania or depression with psychotic features must be ruled out.
MANAGEMENT
Hospitalization may be necessary to protect the patient. Treatment
with antipsychotics is common, although the condition is by
definition self-limited, and no specific treatment is required. The
containing environment of the hospital milieu may be sufficient to
help the patient recover.
DELUSIONAL DISORDER
Delusional disorder is characterized by delusions lasting 1 month
or more without other psychotic symptoms. It is rare, its course is
long term, and treatment is supportive.
EPIDEMIOLOGY
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DANCE ON STILTS AT THE GIRLS’ UNYAGO, NIUCHI
I see increasing reason to believe that the view formed some time
back as to the origin of the Makonde bush is the correct one. I have
no doubt that it is not a natural product, but the result of human
occupation. Those parts of the high country where man—as a very
slight amount of practice enables the eye to perceive at once—has not
yet penetrated with axe and hoe, are still occupied by a splendid
timber forest quite able to sustain a comparison with our mixed
forests in Germany. But wherever man has once built his hut or tilled
his field, this horrible bush springs up. Every phase of this process
may be seen in the course of a couple of hours’ walk along the main
road. From the bush to right or left, one hears the sound of the axe—
not from one spot only, but from several directions at once. A few
steps further on, we can see what is taking place. The brush has been
cut down and piled up in heaps to the height of a yard or more,
between which the trunks of the large trees stand up like the last
pillars of a magnificent ruined building. These, too, present a
melancholy spectacle: the destructive Makonde have ringed them—
cut a broad strip of bark all round to ensure their dying off—and also
piled up pyramids of brush round them. Father and son, mother and
son-in-law, are chopping away perseveringly in the background—too
busy, almost, to look round at the white stranger, who usually excites
so much interest. If you pass by the same place a week later, the piles
of brushwood have disappeared and a thick layer of ashes has taken
the place of the green forest. The large trees stretch their
smouldering trunks and branches in dumb accusation to heaven—if
they have not already fallen and been more or less reduced to ashes,
perhaps only showing as a white stripe on the dark ground.
This work of destruction is carried out by the Makonde alike on the
virgin forest and on the bush which has sprung up on sites already
cultivated and deserted. In the second case they are saved the trouble
of burning the large trees, these being entirely absent in the
secondary bush.
After burning this piece of forest ground and loosening it with the
hoe, the native sows his corn and plants his vegetables. All over the
country, he goes in for bed-culture, which requires, and, in fact,
receives, the most careful attention. Weeds are nowhere tolerated in
the south of German East Africa. The crops may fail on the plains,
where droughts are frequent, but never on the plateau with its
abundant rains and heavy dews. Its fortunate inhabitants even have
the satisfaction of seeing the proud Wayao and Wamakua working
for them as labourers, driven by hunger to serve where they were
accustomed to rule.
But the light, sandy soil is soon exhausted, and would yield no
harvest the second year if cultivated twice running. This fact has
been familiar to the native for ages; consequently he provides in
time, and, while his crop is growing, prepares the next plot with axe
and firebrand. Next year he plants this with his various crops and
lets the first piece lie fallow. For a short time it remains waste and
desolate; then nature steps in to repair the destruction wrought by
man; a thousand new growths spring out of the exhausted soil, and
even the old stumps put forth fresh shoots. Next year the new growth
is up to one’s knees, and in a few years more it is that terrible,
impenetrable bush, which maintains its position till the black
occupier of the land has made the round of all the available sites and
come back to his starting point.
The Makonde are, body and soul, so to speak, one with this bush.
According to my Yao informants, indeed, their name means nothing
else but “bush people.” Their own tradition says that they have been
settled up here for a very long time, but to my surprise they laid great
stress on an original immigration. Their old homes were in the
south-east, near Mikindani and the mouth of the Rovuma, whence
their peaceful forefathers were driven by the continual raids of the
Sakalavas from Madagascar and the warlike Shirazis[47] of the coast,
to take refuge on the almost inaccessible plateau. I have studied
African ethnology for twenty years, but the fact that changes of
population in this apparently quiet and peaceable corner of the earth
could have been occasioned by outside enterprises taking place on
the high seas, was completely new to me. It is, no doubt, however,
correct.
The charming tribal legend of the Makonde—besides informing us
of other interesting matters—explains why they have to live in the
thickest of the bush and a long way from the edge of the plateau,
instead of making their permanent homes beside the purling brooks
and springs of the low country.
“The place where the tribe originated is Mahuta, on the southern
side of the plateau towards the Rovuma, where of old time there was
nothing but thick bush. Out of this bush came a man who never
washed himself or shaved his head, and who ate and drank but little.
He went out and made a human figure from the wood of a tree
growing in the open country, which he took home to his abode in the
bush and there set it upright. In the night this image came to life and
was a woman. The man and woman went down together to the
Rovuma to wash themselves. Here the woman gave birth to a still-
born child. They left that place and passed over the high land into the
valley of the Mbemkuru, where the woman had another child, which
was also born dead. Then they returned to the high bush country of
Mahuta, where the third child was born, which lived and grew up. In
course of time, the couple had many more children, and called
themselves Wamatanda. These were the ancestral stock of the
Makonde, also called Wamakonde,[48] i.e., aborigines. Their
forefather, the man from the bush, gave his children the command to
bury their dead upright, in memory of the mother of their race who
was cut out of wood and awoke to life when standing upright. He also
warned them against settling in the valleys and near large streams,
for sickness and death dwelt there. They were to make it a rule to
have their huts at least an hour’s walk from the nearest watering-
place; then their children would thrive and escape illness.”
The explanation of the name Makonde given by my informants is
somewhat different from that contained in the above legend, which I
extract from a little book (small, but packed with information), by
Pater Adams, entitled Lindi und sein Hinterland. Otherwise, my
results agree exactly with the statements of the legend. Washing?
Hapana—there is no such thing. Why should they do so? As it is, the
supply of water scarcely suffices for cooking and drinking; other
people do not wash, so why should the Makonde distinguish himself
by such needless eccentricity? As for shaving the head, the short,
woolly crop scarcely needs it,[49] so the second ancestral precept is
likewise easy enough to follow. Beyond this, however, there is
nothing ridiculous in the ancestor’s advice. I have obtained from
various local artists a fairly large number of figures carved in wood,
ranging from fifteen to twenty-three inches in height, and
representing women belonging to the great group of the Mavia,
Makonde, and Matambwe tribes. The carving is remarkably well
done and renders the female type with great accuracy, especially the
keloid ornamentation, to be described later on. As to the object and
meaning of their works the sculptors either could or (more probably)
would tell me nothing, and I was forced to content myself with the
scanty information vouchsafed by one man, who said that the figures
were merely intended to represent the nembo—the artificial
deformations of pelele, ear-discs, and keloids. The legend recorded
by Pater Adams places these figures in a new light. They must surely
be more than mere dolls; and we may even venture to assume that
they are—though the majority of present-day Makonde are probably
unaware of the fact—representations of the tribal ancestress.
The references in the legend to the descent from Mahuta to the
Rovuma, and to a journey across the highlands into the Mbekuru
valley, undoubtedly indicate the previous history of the tribe, the
travels of the ancestral pair typifying the migrations of their
descendants. The descent to the neighbouring Rovuma valley, with
its extraordinary fertility and great abundance of game, is intelligible
at a glance—but the crossing of the Lukuledi depression, the ascent
to the Rondo Plateau and the descent to the Mbemkuru, also lie
within the bounds of probability, for all these districts have exactly
the same character as the extreme south. Now, however, comes a
point of especial interest for our bacteriological age. The primitive
Makonde did not enjoy their lives in the marshy river-valleys.
Disease raged among them, and many died. It was only after they
had returned to their original home near Mahuta, that the health
conditions of these people improved. We are very apt to think of the
African as a stupid person whose ignorance of nature is only equalled
by his fear of it, and who looks on all mishaps as caused by evil
spirits and malignant natural powers. It is much more correct to
assume in this case that the people very early learnt to distinguish
districts infested with malaria from those where it is absent.
This knowledge is crystallized in the
ancestral warning against settling in the
valleys and near the great waters, the
dwelling-places of disease and death. At the
same time, for security against the hostile
Mavia south of the Rovuma, it was enacted
that every settlement must be not less than a
certain distance from the southern edge of the
plateau. Such in fact is their mode of life at the
present day. It is not such a bad one, and
certainly they are both safer and more
comfortable than the Makua, the recent
intruders from the south, who have made USUAL METHOD OF
good their footing on the western edge of the CLOSING HUT-DOOR
plateau, extending over a fairly wide belt of
country. Neither Makua nor Makonde show in their dwellings
anything of the size and comeliness of the Yao houses in the plain,
especially at Masasi, Chingulungulu and Zuza’s. Jumbe Chauro, a
Makonde hamlet not far from Newala, on the road to Mahuta, is the
most important settlement of the tribe I have yet seen, and has fairly
spacious huts. But how slovenly is their construction compared with
the palatial residences of the elephant-hunters living in the plain.
The roofs are still more untidy than in the general run of huts during
the dry season, the walls show here and there the scanty beginnings
or the lamentable remains of the mud plastering, and the interior is a
veritable dog-kennel; dirt, dust and disorder everywhere. A few huts
only show any attempt at division into rooms, and this consists
merely of very roughly-made bamboo partitions. In one point alone
have I noticed any indication of progress—in the method of fastening
the door. Houses all over the south are secured in a simple but
ingenious manner. The door consists of a set of stout pieces of wood
or bamboo, tied with bark-string to two cross-pieces, and moving in
two grooves round one of the door-posts, so as to open inwards. If
the owner wishes to leave home, he takes two logs as thick as a man’s
upper arm and about a yard long. One of these is placed obliquely
against the middle of the door from the inside, so as to form an angle
of from 60° to 75° with the ground. He then places the second piece
horizontally across the first, pressing it downward with all his might.
It is kept in place by two strong posts planted in the ground a few
inches inside the door. This fastening is absolutely safe, but of course
cannot be applied to both doors at once, otherwise how could the
owner leave or enter his house? I have not yet succeeded in finding
out how the back door is fastened.