NHPC BASLP cheat sheet

Outer ear: pinna and external auditory canal (about 2.5 cm in adults) resonate near 2–4 kHz, giving roughly 10–15 dB gain in that region; canal terminates at the tympanic membrane.

Middle ear transformer: ossicular lever plus areal ratio (tympanic membrane ≈55 mm² to stapes footplate ≈3.2 mm², ratio ≈17:1) yields about 25–30 dB pressure gain; impedance matching is its main function.

Eustachian tube equalizes middle-ear pressure; in infants it is shorter, more horizontal, and more compliant, predisposing to otitis media.

Cochlea: ~2.5 turns; basilar membrane is narrow and stiff at the base (high frequencies) and wide and floppy at the apex (low frequencies) - tonotopic organization.

Organ of Corti: one row of inner hair cells (~3,500, afferent sensory) and three rows of outer hair cells (~12,000, electromotile amplifiers); stereocilia deflection toward the tallest row depolarizes hair cells via tip-link tension.

Endocochlear potential: stria vascularis generates about +80 mV in scala media; hair cell resting potential about −40 to −70 mV, driving the transduction current.

Auditory pathway: spiral ganglion → cochlear nucleus → superior olivary complex (first binaural interaction) → lateral lemniscus → inferior colliculus → medial geniculate body → auditory cortex.

Speech subsystems: respiration (power), phonation (larynx, vocal folds), resonation (pharyngeal/oral/nasal cavities), articulation (tongue, lips, palate); vocal folds vibrate via myoelastic-aerodynamic (Bernoulli) action.

Broca area (inferior frontal gyrus, dominant hemisphere) supports motor speech and expressive language; damage produces nonfluent aphasia with relatively preserved comprehension.

Wernicke area (posterior superior temporal gyrus) supports auditory comprehension; damage produces fluent aphasia with poor comprehension and impaired repetition.

Arcuate fasciculus connects Wernicke to Broca; lesion yields conduction aphasia - fluent speech, good comprehension, markedly impaired repetition.

Cranial nerves for speech/swallowing: V (trigeminal, mastication), VII (facial, lips), IX (glossopharyngeal), X (vagus, palate/vocal folds via recurrent laryngeal nerve), XII (hypoglossal, tongue).

Upper motor neuron lesions cause spastic dysarthria with hyperreflexia and pseudobulbar signs; lower motor neuron lesions cause flaccid dysarthria with atrophy and fasciculations.

Cerebellar damage produces ataxic dysarthria: irregular articulatory breakdown, excess and equal stress, harsh voice; basal ganglia damage produces hypokinetic (Parkinson) or hyperkinetic dysarthria.

Left hemisphere is dominant for language in ~95% of right-handers and ~70% of left-handers; right hemisphere contributes prosody, pragmatics, and discourse.

Dementia of the Alzheimer type: early anomia and impaired episodic memory with relatively spared syntax; primary progressive aphasia is a neurodegenerative language disorder distinct from stroke aphasia.

dB SPL = 20 log10(P/P0), P0 = 20 µPa; dB HL reference is the normative threshold SPL at each frequency, so 0 dB HL differs in SPL across frequencies.

Doubling sound pressure = +6 dB; doubling power = +3 dB; doubling distance from a point source in free field ≈ −6 dB.

Pure tone = single frequency; complex periodic sounds have a fundamental plus harmonics; noise has energy spread across a band (white = equal energy per Hz).

Resonance: a tube closed at one end has quarter-wavelength resonances; adult male vocal tract (~17 cm) has first formant near 500 Hz, female (~14 cm) near 700 Hz.

Vowels are identified by formant frequencies (F1 inversely related to tongue height, F2 related to tongue frontness); consonant place cues include burst spectra, formant transitions, and VOT.

Fourier analysis decomposes a waveform into sinusoidal components; the spectrum shows amplitude by frequency, the spectrogram shows time × frequency × intensity.

Masking: simultaneous masking is greatest when masker is near the signal frequency; upward spread of masking means low-frequency maskers mask higher-frequency signals more than the reverse.

Just-noticeable difference in frequency is ~1–3 Hz below 1 kHz and roughly 0.2–0.3% above 1 kHz; temporal integration time constant is about 100–200 ms.

Pure-tone audiometry: air conduction 125–8000 Hz, bone conduction 250–4000 Hz; test-retest reliability ±5 dB; threshold is lowest level heard in ≥50% of ascending trials.

Conductive loss: air-bone gap >10 dB with normal bone conduction; sensorineural loss: air and bone thresholds equal; mixed: both elevated with a gap.

Degree (adults): normal ≤25 dB HL, mild 26–40, moderate 41–55, moderately severe 56–70, severe 71–90, profound >90 dB HL.

Tympanometry: Type A peak 0.3–1.5 mmho at ±100 daPa; Type B flat (effusion or perforation); Type C peak < −100 daPa (negative pressure); Type As low compliance; Type Ad high compliance.

Acoustic reflex: stapedius contraction at ~70–100 dB SL; absent reflex with present OAE suggests retrocochlear involvement; reflex decay >50% in 10 s at 500/1000 Hz is abnormal.

OAEs: TEOAE present in normal ears up to ~30 dB HL; absent DPOAE at high frequencies suggests cochlear (outer hair cell) loss; OAEs are present despite mild neural loss.

ABR: wave I distal VIII nerve, wave III cochlear nucleus, wave V inferior colliculus/lateral lemniscus; interpeak I–V >4.4 ms or interaural wave V difference >0.2 ms warrants retrocochlear workup.

Behavioral tests for central auditory processing: dichotic digits, competing sentences, gaps-in-noise, pitch pattern; diagnose only when deficits are not explained by peripheral loss or cognition.

Hearing aid gain target: NAL-NL2 and DSL v5 are common prescriptive methods; verify with real-ear measurement (REM) to within ±5 dB of target, not by manufacturer default.

Insertion gain = aided ear canal SPL minus unaided ear canal SPL at the same reference point; real-ear aided response (REAR) is compared to prescriptive target.

Compression: WDRC (wide dynamic range compression) suits sensorineural loss; attack/release times trade off audibility vs. distortion; knee point separates linear from compressed regions.

Feedback management: reduce venting, ensure proper dome/mold fit, use feedback cancellation; occlusion effect is worst for <500 Hz with small vents.

Cochlear implant candidacy (adults): moderate-to-profound bilateral SNHL with limited benefit from appropriately fitted hearing aids; aided speech perception scores guide candidacy.

Pediatric habilitation: early identification (1-3-6: screen by 1 month, diagnose by 3, intervene by 6), family-centered therapy, LSLS or bilingual-bicultural approaches.

Aural rehabilitation: communication strategies training, speechreading, assistive listening devices (FM/loop systems), environmental modification, and counseling on realistic expectations.

Outcome measures: COSI, HHIE/HHIA, APHAB, and speech-in-noise testing quantify benefit and guide fine-tuning.

Speech sound disorder classification: articulation (motor production), phonological (rule-based pattern errors, e.g., final consonant deletion, fronting, stopping), and childhood apraxia of speech (inconsistent errors, groping, impaired sequencing).

Language sample analysis: MLU in morphemes, type-token ratio, mean length of utterance norms (e.g., ~1.0 at 12–18 months, ~2.0 at 24 months, ~3.0 at 36 months).

Standardized assessment: report standard scores (mean 100, SD 15), percentile ranks, and confidence intervals; a score below −1.5 to −2 SD indicates significant delay.

Aphasia classification by fluency, comprehension, and repetition: Broca (nonfluent, good comprehension, poor repetition), Wernicke (fluent, poor comprehension and repetition), conduction (fluent, good comprehension, poor repetition), anomic, global, transcortical.

Dysarthria vs. apraxia: dysarthria reflects neuromuscular execution deficits (consistent, affects all speech tasks); apraxia reflects planning/programming (inconsistent, worse with complexity, islands of fluent speech).

Voice assessment: acoustic (jitter, shimmer, harmonics-to-noise ratio), aerodynamic (maximum phonation time, s/z ratio), perceptual (GRBAS, CAPE-V), and laryngeal imaging.

Fluency assessment: count stuttered syllables vs. total syllables; >3% stuttered syllables in connected speech is typically disordered; assess secondary behaviors and avoidance.

Dysphagia: bedside swallow exam plus instrumental assessment (VFSS, FEES); signs include coughing, wet voice, residue, and silent aspiration.

Evidence-based intervention principles: target functional communication, use high-intensity massed practice for motor speech, and embed goals in natural contexts for language intervention.

Speech sound intervention approaches: traditional articulation (isolation→syllable→word→phrase→sentence→conversation), phonological (minimal pairs, cycles, maximal oppositions), and motor-based (PROMPT, DTTC) for CAS.

Aphasia intervention: constraint-induced language therapy, melodic intonation therapy for nonfluent aphasia, semantic feature analysis for anomia, and conversational coaching for pragmatics.

Stuttering management: fluency shaping (easy onset, light contact, prolonged speech) vs. stuttering modification (cancellation, pull-out, preparatory set); Lidcombe program for preschool children.

Autism intervention: naturalistic developmental behavioral interventions (ESDM, JASPER), visual supports, and AAC; target joint attention and social communication.

AAC decision-making: consider unaided (signs, gestures) and aided (SGD, picture boards) systems; model use by communication partners and match vocabulary to the user's needs.

Dysarthria management: rate control, breath support, articulation drills, and compensatory strategies; for severe cases consider AAC or voice amplification.

Dementia care: spaced retrieval, errorless learning, memory books, and caregiver training; focus on functional communication and quality of life.

ASHA Code of Ethics: four principles (beneficence/nonmaleficence, responsibility, integrity, respect); informed consent and confidentiality are core obligations.

Scope of practice: SLPs and audiologists practice within their competence; supervise assistants appropriately and refer when outside expertise.

HIPAA protects protected health information; FERPA governs educational records; obtain written release before sharing client information.

IDEA (Individuals with Disabilities Education Act): free appropriate public education, least restrictive environment, IEP, and procedural safeguards; Part C covers children under 3 (IFSP).

Section 504 of the Rehabilitation Act and the ADA prohibit disability discrimination and require reasonable accommodations.

Early Hearing Detection and Intervention (EHDI) 1-3-6 benchmarks: screening by 1 month, diagnosis by 3 months, intervention by 6 months.

Licensure and certification: state licensure, ASHA CCC, and continuing education requirements; documentation must be accurate, timely, and legible.

Cultural competence and equity: use interpreters, culturally appropriate assessment tools, and avoid over-identification or under-identification of diverse populations.

EBP triad: best available research evidence, clinical expertise, and client values/preferences; levels of evidence rank systematic reviews and RCTs above cohort, case-control, and expert opinion.

Study designs: RCT (randomization, control), quasi-experimental (no random assignment), cohort (follows exposed/unexposed), case-control (retrospective, compares outcome groups), single-subject designs (ABA, multiple baseline).

Validity: internal validity (causal inference) vs. external validity (generalizability); threats include selection bias, attrition, and instrumentation.

Reliability: test-retest, inter-rater, and internal consistency (Cronbach's alpha ≥0.70 acceptable); standard error of measurement quantifies score precision.

Sensitivity = true positives/(true positives + false negatives); specificity = true negatives/(true negatives + false positives); positive predictive value depends on prevalence.

Descriptive statistics: mean, median, mode, standard deviation; inferential tests: t-test (two groups), ANOVA (three or more), chi-square (categorical), correlation (Pearson r).

p-value is the probability of the observed result under the null hypothesis; α = 0.05 is conventional; statistical significance does not equal clinical significance.

Effect size: Cohen's d (0.2 small, 0.5 medium, 0.8 large); confidence intervals communicate precision better than p-values alone.